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Year : 1986  |  Volume : 34  |  Issue : 1  |  Page : 19-23

Ocular lesions in Hansen's (leprosy)

A 19/1, D.R.O. Colony Natham Road, Madurai, India

Correspondence Address:
A Samuel Gnanadoss
A 19/1, D.R.O. Colony Natham Road, Madurai 625007
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Source of Support: None, Conflict of Interest: None

PMID: 3443494

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How to cite this article:
Gnanadoss A S, Rajendran N. Ocular lesions in Hansen's (leprosy). Indian J Ophthalmol 1986;34:19-23

How to cite this URL:
Gnanadoss A S, Rajendran N. Ocular lesions in Hansen's (leprosy). Indian J Ophthalmol [serial online] 1986 [cited 2021 Jul 30];34:19-23. Available from: https://www.ijo.in/text.asp?1986/34/1/19/26350

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Table 2

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Table 1

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Table 1

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Hansen's disease is quite rampant in India. Still, for the magnitude of its occurrence, the number of Indian reports dealing with its ocular complications is quite a few only[1],[2],[3],[4] So a survey was done to study this disease with special refer­ence to certain stated facts about ocular lesions in Hansen's, viz , the incidence being more in lepromatous type[5],[6], the ocular involvement occurring late in the disease[7],[8], loss of vision being seen in comparatively a few cases only[8],[9],[10]. Following is an analy­sis of this study.

  Materials and methods Top

The cases analysed here were the inmates of the Government Leprosy Rehabilitation Home near Madurai.

Leprologist's opinion was obtained regar­ding systemic disease. History elicitation included the duration and treatment of Hansen's and any ocular problem the patients had.

Ocular examination included oblique and biomicroscopy assessment, fundus examina­tion, tonometry and vision check. Refrac­tive errors were corrected. Those who needed surgery were operated upon.

  Observations and discussion Top

In this study 250 cases were analysed.

Out of them, 102 cases (40.8%) were lepro­matous, 96 (38.3%) were tuberculoid and 52 were (20.8%) borderline cases. Since Hansen's is a chronic condition it is not surprising to see that 52% were above the age of 40 years. Out of these 250 cases, 148 (59.2°0) showed ocular lesions-an incide­nce congruous with 47% of Weekeroons[11]; but is lower than that of Harley (90%)[12]; Lamba & Santosh Kumar. (87.3%).[4] Hornblass (76%)[13], Malla et al (74.2%)[14] Ticho & Sira[15] give a very low figure of 6.3%. This variation can be racial too[11],[12] Asiatics being more susceptible[16].

Ocular Adnexa :- Madarosis was seen in 28 cases (11.2%). Out of the 32 cases of lagophthalmos, 20 were seen in Tuberculoid type, seven in lepromatous and five in borderline types. This predominence of lid affection in tuberculoid type is a known fact[17]. But others[14],[16] have found equal distribution amongst all types. [Table - 1]

It is interesting to note that Krassai[18] has found logophthalmos to be the second common cause for blindness. Lamba & Santosh Kumar[19] have mentioned this to be a sight threatening lesion.

Fortynine cases had definite chronic conjunctivitis with symptoms. This inciden­ce (19.6%) is high. Six cases below the age of 40 had fleshy pterygium-four being bilateral and two being unilateral. This rarity has been reported in literature[14].

Cornea : Corneal lesions were the commonest (25.2%) Hornblass[13] (1973) figure is higher than this-61%. Symptoms were minimal, most probably due to anaesthesia[20]. [Table - 2].

The typical chalky white deposits were seen in three cases. Two of the 25 cases of exposure keratitis were of acute in nature requiring tarsorrhaphy. All cases of I.K. were unilateral and sectorial in distribution. Three in the superotemporal and one in temporal quadrants. Bullous keratopathy was secondary to iridocyclitis which had caused corneal endothelial damage. Apart from exposure keratitis, 70% of the remain­ing lesions were seen in lepromatous type. Corneal sensation was reduced or absent in 101 cases (40.4%)-an incidence higher than that in literature[14]. sub It was seen even in the absence of any other lesions. Allen & Byers[19] considered it as the earliest sign of ocular involvement. Total anaesthesia is usually rare in Hansen's[10],[20]

Leproma was seen in 7 cases. Primary corneal involvement is said to be not a serious one [19,[21].

The three cases of scleritis cleared up with treatment without sequelae. Primary involvement of this tissue is rare[3].

Uveitis was seen in 14 cases (5.6%) of lepromatous Hansen's. Incidence met with by other authors ranges from 9 to 16%[3],[8],[13] . Acute symptoms were not met with. Four of these cases exhibited non-granulomatous type of iritis; while ten were of granulo­matous type. Lepra pearls were seen in two cases. Eight cases showed iris atrophy which is considered to be neurotrophic in origin[6].

Iritis is said to be the common cause for blindness in Hansen's[21],[22].

The cataracts (except the post iritic) met with in this study were of senile type. The age of occurrence was in no way different from the normal group. Others[4],[11],[23] have also opined that there is no true leprotic cataract. Four cases showed post-iridocy­clitic cataract.

In 120 adult Hansen's cases without any other ocular lesions, the ocular tension was elevated in only five cases (4.2%). This approximates to the value seen in normal population. It is said that decreased aqueous secretion in Hansen's is the cause for rarity of primary glaucoma[10],[14].

Three of the iridocyclitic cases showed elevated tension.

Excluding that of cataract, presbyopia and aphakia, it was found that myopia (19 cases) and hypermetropia (17 cases) were equally distributed in this study. This closely approximates to the curves of Schee­rer and Betsch. Assessment of presbyopia did not show any early onset, as is alleged[24].

Leprosy rarely affects the fundus[1],[25] and in this series fundus lesion pertaining to Hansen's was not seen in any case.

From the above table it can be inferred that ocular lesions occur only later in the disease process. Dethlef[8] has found this period to be 7.2 years. This can be anywhere ­from sixe[26] to 20 years[14]. [Table - 3]

About the efficacy of systemic treatment on prevention of ocular involvement, it is observed that it is the institution of early treatment that is effective in preventing ocu­lar lesions in Hansen's, a view concurring with that of Mclaren et al[17] [Table - 4]

Cataract surgery was done in twenty cases of senile cataract. Intracapsular extrac­tion (using cryo) with sector iridectomy was carried out. The surgery and postoperative period were uneventful. The wound healing was good. In all cases complication was not encountered and the visual improvement was comparable with that of normal cases.

This good result after ocular surgery in Hansen's patients confirms [the findings of other authors[4],[5],[27],[28].

There are various factors causing reduc­tion of vision to less than 6/60 (excluding senile cataract [Table - 5]. Amongst these 43 cases, 40 were lepromatous type and three were tuberculoid type. Total loss of vision was seen in 11 cases (4.8%)-seven of them due to chronic iridocyclitis. This had caused defective vision by complication such as cataract, occlusiopupilae, glaucoma and bullous keratopathy.

In Leprosy, visual loss is not as high as thought of 4% (Dethelfs[8]), 5% (Damato[9]); 10% (Shield et al[10]). It is seen in long stand ing cases only[22]. As expected, lepromatous type causes blindness much more commonly than Tuberculoid type (Ten out of 11 cases)---a finding observed by Ffytche[16] too.

  Summary Top

In 250 Hansen's cases assessed, ocular lesions were seen in 59.2% of cases. Cornea was more frequently involved (25.2%). Excluding lagophthalmos, most of the lesions were seen in lepromatous cases of long duration. Unless systemic treatment is instituted early, this does not prevent development of ocular lesions. Posterior segment was uninvolved. Ocular tension and refractive status were that of normal population. Operations were attended with good results. Visual loss, which was seen in 4.8% of cases, was due either to corneal or to uveal lesions.

  References Top

Balakrishnan, E.J., 1966, J. All India Ophthal­mol, Soc. 14 :214.  Back to cited text no. 1
Acharya, B.P., 1978, Ind. J. Ophthalmol. 21 : 24.   Back to cited text no. 2
Prasad, S.B., 1981, J. Indian Med. Assn. 76: 158  Back to cited text no. 3
Lamba, P.A. & Santosh Kumar, D., 1984, Ind. J. Ophthalmol. 32: 61.  Back to cited text no. 4
Choyce O.P., 1969, Brit. J. Ophthalmol 53: 2 17  Back to cited text no. 5
Slem G., 1971, Amer. J. Ophthalmol. 71 :431­-434.  Back to cited text no. 6
Me. Laren et al., 1961, Int. J. Leprosy, 29 : 20.   Back to cited text no. 7
Dethleff, R., 1981. Brit. J. Ophthalmol. 65 : 223.   Back to cited text no. 8
Damato, F.J., 1960, Brit. J. Ophthalmol 44: 164.  Back to cited text no. 9
Shields. J.A. et al, 1974, Amer. J. Ophthalmol. 77 : 880.  Back to cited text no. 10
Weekeroon, L., 1969, Brit. J. Ophthalmol, 53 : 466.  Back to cited text no. 11
Harley, R.D., 1946, Amer. J. Ophthalmol. 29 295.  Back to cited text no. 12
Hornblass, A., 1973, Amer. J. Ophthalmol. 75. 478.  Back to cited text no. 13
Malla, O.K. et al, 1981. Brit. J. Ophthalmol. 65 : 226.  Back to cited text no. 14
Ticho, U. & Sira. B., 1970, Brit. J. Ophthal­mol. 54:107.  Back to cited text no. 15
Ffytche, T.J., 1981, Lepr. Rev. 52: 111  Back to cited text no. 16
Duke-Elder, S., 1965, "System of Ophthalmo­logy", Vol VIII-2, Henry Kimpton, p. 845.  Back to cited text no. 17
Krassai, A., 1970, Int. J. Lepr. 38 : 422.  Back to cited text no. 18
Allen, J.H. Byer, J.L., 1960, Arch. Ophthal­mol. 64: 216.  Back to cited text no. 19
Weekeroon, L., 1972, Birt. J. Ophthalmol. 56: 106.  Back to cited text no. 20
Ffytche, T.J., 1981, Trans. Ophthal. Soc. U.K. 101 : 325.  Back to cited text no. 21
Hogeweg, M. & Leiker, D.L., 1983, Brit. J. Dermat. 109: 477.  Back to cited text no. 22
Holmes, W.J., 1957, Trans. Ophthalmol. Soc. U.K., 81 : 397.  Back to cited text no. 23
24, Wood, D.J., 1925, Brit. J. Ophthalmol. 9:1.  Back to cited text no. 24
Lamba, P.A. & Srinivasan, R., 1983, Leprosy India, 55 : 209.  Back to cited text no. 25
Richards, W.W. & Arrington, J.M., 1969, Amer. J. Ophthalmol. 68 :492.  Back to cited text no. 26
Kennedy, P.J., 1952, Amer. J. Ophthalmol. 35 1360.  Back to cited text no. 27
Panneerselvam, V., 1986, J1. Madras State Ophthal. Assn. (In print).  Back to cited text no. 28


  [Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5]

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