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   Table of Contents      
ARTICLES
Year : 1983  |  Volume : 31  |  Issue : 6  |  Page : 781-784

Diagnostic problems in ocular hypertension


Dr. Rajendra Prasad Centre for Ophthalmic Sciences All-India Institute of Medical Sciences Ansari Nagar, New Delhi, India

Correspondence Address:
N N Sood
Dr. Rajendra Prasad Centre for Ophthalmic Sciences All-India Institute of Medical Sciences Ansari Nagar, New Delhi
India
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Source of Support: None, Conflict of Interest: None


PMID: 6676267

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How to cite this article:
Sood N N, Grover A K, Agarwal H C. Diagnostic problems in ocular hypertension. Indian J Ophthalmol 1983;31:781-4

How to cite this URL:
Sood N N, Grover A K, Agarwal H C. Diagnostic problems in ocular hypertension. Indian J Ophthalmol [serial online] 1983 [cited 2020 Jun 4];31:781-4. Available from: http://www.ijo.in/text.asp?1983/31/6/781/29325

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Ocular hypertension was a by product of the glaucoma surveys which revealed a large population with higher than statistically nor­mal intraocular pressures, without any signs of field or disc changes.[1],[2] Perkins[3] defined ocular hypertenision as an intraocular pressure equal to or' greater than 22 mm. Hg in one or both eyes as measured by applanation tonometry on two or more occasions with no glaucomat­ous field defects, an open angle and no history suggestive of closed angle glaucoma. Numer­ous studies on the subject have appearred in the world literatrure, but to the best of our knowledge, no work on ocular hypertension is available from India.


  MATERIAL & METHODS Top


90 patients with a preliminary diagnosis of ocular hypertension, referred to the Glaucoma clinic on the basis of a schiotz re­cording of 3/5.5 gm. or 5.5/7.5 gm. weight or less with normal discs and normal chamber depth were included in the study. The patients were subjected to a full glaucoma work up which included a detailed history (including a history of use of steroids, family history and history of any systemic illness), refraction, re­peated Goldmann applanation tonometry, exclusion of abnormal scleral rigidity, gonios­copy and exclusion of presence of diabetes and Goldmann perimetry. Selected subjects were subjected to monitoring of diurnal variation of intraocular pressure, water drinking test, out­flow facility and colour fundus photography.


  Observations Top


Only 69 out of the 90 patients referred with a provisional diagnosis of ocular hypertension were established to be ocular hypertensives at the conclusion of investigations.[Table - 1]

Age & sex distribution

The age & sex distribution is shown in [Table - 2] .

Family history of open angle glaucoma was obtained in 13 of the patients (18.8%).

16 of the patients we're either known diabe­tics or detected to be diabetic on screening (23.2%)

Other systemic problems

10 patients had systemic problems other than diabetes mellitus. 7 patients were hyper tensive, 2 had coronary artery disease (one hypertensive) and 2 had cerebro vascular dis­ease (both hypertensive). One patient has hypothyroidism and one showed maniac de­pressive psychosis.

Intraocular pressure: [Table - 3]

Myopia:

13 of the patients were myopic (18.8%) 3(4.3%) of these had a myopia of mrore than 6 diopters.

Pseudo Exfoliation:

was present in one patient (both eyes) (1:56% of the eyes).

One patient had a super-temporal branch vein block.


  Discussion Top


The glaucoma surveys have established that the intraocular pressure distribution kin the general population does not follow a normal Gaussian curve but shows a distinct skewing of the curve towards the higher pressure levels. However, the diagnosis of ocular hyperten­sion by surveys in general population has a number of inherent drawbacks. Besides the expense of immense effort that it involves, a number of subject could be missed because of the known diurnal[4] and long term cyclical 5 var­iations in intraocular pressure.

A wrong diagnosis of ocular hypertension (false positives) can result from a number of factors. The most importatnt causes of exclu­sion of cases provisionally labelled as ocular hypertensives was non reproductibility of high intraocular pressure recording on subsequent repeated applanation tonometry. This could possibly be due to a fallacious schiotz to­nometric recording, which could be a result of an instrumental error, an uncooperative pa­tient or operator errors. A high scleral rigidity was the cause of high schiotz tonometry re­cording in one of the patients. A thorough biomicroscopic examination and gonioscopy must be done to exclude cases of glaucoma secondary to uveitis and angle closure glaucoma. Goldmann perimetry picked up glaucomatous defects in two subjects, whose discs were clinically assessed to be physiologi­cal, thus excluding them from the definition of ocular hypertension. Another important cause to be excluded is the steroid induced ocular hypertension. A history which suggested steroid induced rise of pressure was obtained in three subjects in our series, suggesting the importance of this entity. To­nography can exclude the rare patient of hypersecretion glaucoma who may also pre­sent with a clinical picture akin to ocular hypertension. excluded is the steroid induced ocular hypertension. A history which suggested steroid induced rise of pressure was obtained in three subjects in our series suggesting the importance of this entity. To­nography can exclude the rare patient of hypersecretion glaucoma who may also pre­sent with a clinical picture skin to ocular hypertension.

A significant number of patients in the study (14.5%) were in the fourth decade. The obser­vations could suggest the earlier occurrence of raised introcular pressure in Indians and the importance of including this age group in glaucoma surveys. An equal number of males and females were diagnosed as ocular hyper­tensive in the present study. A number of studies from abroad report significantly high mean intraocular pressure values in women then in men, while other fail to find such a sex difference.

A high rate of positive family history of glaucoma (18.8%) and prevalence of diabetes mellitus (23.2%) has been observed in this study. This could partially be a result of the fact that the coular hypertensives have been picked up from a hospital, rather than from a survey in general population. However, a genetic component to the inheritance of ocular hypertension has been pointed out.[6] A number of studies have shown an association of increased intraocular pressure with juvenile diabetes as well as the adult onset diabetes. The ocular hypertensives in the Framingham Eye study[7] had a higher range of mean casual blood sugars (1.5 - 22.5 mg./ml.) than the com­parable age and sex normotensive control groups.

The distribution of intraocular pressure in the ocular hypertensives in this study showed 32.8% with a pressure of less than 25 mm. Hg and 71.9% of less than 30 mm. Hg. It is this large group of patients who constitute a dif­ficult problems both from the point of view of diagnosis and the decision regarding manage­ment.

The diagnosis of ocular hypertension must only be made after a careful history taking and extensive glaucoma work up. A number of dif­ficulties and pitfalls must be consciously av­oided in arriving at the diagnosis.


  Summary Top


90 patients with a preliminary diagnosis of ocular hypertension poresenting to this glaucoma clinic were included in a prospective study. Preliminary referral was based on a high schiotz tonometric recording (of 5/5.5 gm. or 5.5/7.5 gm. wt. or less in the O.P.D. with normal discs & normal chamber depth. The patients were subjected to a full glaucoma work up. The final diagnosis of ocular hyper­tension was based on a minimum of two appla­nation readings of more than 21 mm. of Hg on different occasions.

23% of the patients were detected to be diabetic. Vertical studies on these cases are in progress and nearly 40% of the cases have a follow up of over 1 year. Studies with a longer follow up period and at a number of different centres need to be undertaken.

 
  References Top

1.
Linner, E. and Stromberg, U. 1967 In W Leydhecker (Ed.) Glaucomas Tutzing Symposium. Basal Karger, P 187.  Back to cited text no. 1
    
2.
Hollows, F.C., and Graham, P.A. 1966 Brit, J Ophthalmol. 50:570  Back to cited text no. 2
    
3.
Perkins, E.S. 1966 Trans. Ophthalmol Sec. U.K 86:199.  Back to cited text no. 3
    
4.
Kitazawa Y. Horie T. 1979 Glaucoma Update - Berlin, Heidelberg, New York, Springer Verlag: 169-176.  Back to cited text no. 4
    
5.
Stromberg U. 1962 Acta ophthalmol (kha.) Suppl 69.  Back to cited text no. 5
    
6.
Armaly, M.F. 1965 Arch. Ophthalmol. 73:11-18.  Back to cited text no. 6
    
7.
Kawn, HA, Leibowitz, HM, GanleyJ.P. 1977 Am.J Bpidemiol 106:33-41.  Back to cited text no. 7
    



 
 
    Tables

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



 

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MATERIAL & METHODS
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Discussion
Summary
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