Glyxambi
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 
  • Users Online: 2049
  • Home
  • Print this page
  • Email this page


 
   Table of Contents      
ARTICLE
Year : 1964  |  Volume : 12  |  Issue : 1  |  Page : 15-18

Arsenical optic atrophy


Muslim University, Institute of Ophthalmology, Aligarh, India

Date of Web Publication13-Feb-2008

Correspondence Address:
B R Shukla
Muslim University, Institute of Ophthalmology, Aligarh
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


Rights and Permissions

Clinical trial registration None

Rights and Permissions

How to cite this article:
Shukla B R, Ahuja O P, Paul S D. Arsenical optic atrophy. Indian J Ophthalmol 1964;12:15-8

How to cite this URL:
Shukla B R, Ahuja O P, Paul S D. Arsenical optic atrophy. Indian J Ophthalmol [serial online] 1964 [cited 2019 Oct 19];12:15-8. Available from: http://www.ijo.in/text.asp?1964/12/1/15/39066

Modern therapeusis armed with the newest of antibiotics has rendered many of the old drug complications obsolete. This statement holds good in countries where rigid laws govern the practice of medicine and the dispensing of drugs.

It is common knowledge that with the introduction of Penicillin and other antibiotics, arsenic and arsenical com­pounds have literally disappeared from the prescription of the modern physi­cians. That, however, is no so in our country where the practices of quacks and ill-trained physicians in antiquated systems of medicine are allowed to continue and even encouraged.

It is, therefore, not uncommon to encounter patients who have been pres­cribed gold compounds, mercurials and arsenicals without any proper follow-up or laboratory facilities, of which our reported case is an example.

Corneal complications following, Ar­senical therapy have been described by Hegner (1917), Kirby (1929), and Hallum (1934). The clinical descrip­tion of a Keratitis sometimes accom­panying exfoliative dermatitis has been mentioned. Kirby labelled his cases of keratitis following arsenic therapy as "Keratitis Exfoliativum" and was of the opinion that there was a patho­logic analogy between the affection of the skin and cornea.

Gresser and Thomas (1942) reported the occurrence of superficial punctate keratitis following arsenic therapy. The disease manifested itself on the ninth day of the commencement of treat­ment.

Involvement of optic nerve following arsenic treatment has been described by Duke-elder (1947). Walsh (1947) re­ported the development of neuro­retinitis in a 30 years old negro woman after receiving arsenic treatment.

Frickman, Hollenhorst and Ammer­mann (1960) reported the development of severe retinopathy with vascular proliferation and vitreous haemorr­hage, following arsenic therapy.

The most dramatic case showing a bilateral, sudden and complete amau­rosis has been reported by Tissot Daquette (1934).

The review of literature thus pre­sents a heterogenous involvement of ocular tissues varying in severity and affection following the arsenic therapy as a complication.

A case suffering from bilateral optic neuritis going on to optic atrophy fol­lowing arsenic therapy is being present­ed in this context.


  Case Report Top


Patient 'C.S.' Hindu male Age-17 years.

Vision (Both eyes)-No perception of light.

Patient was admitted in this hospital following three weeks of arsenic treat­ment which was prescribed for sus­pected eosinophilia. The lay physi­cian gave one injection of Soamin followed by Hetrazan tablets and Acetylarsan injections. The patient became unconscious and remained so for a week. He was then given B A.L. and Achromycine injections.

On recovering consciousness, the patient complained of severe head­ache. This was followed by a sudden bilateral loss of vision 24 hours later

On examination: Nothing abnor­mal was noted in the lids, conjunctiva and cornea.

The pupils of both eyes were dilated and fixed, not reacting to light direct or to consensual stimulation.

Fundus picture (Both eyes) : Slightly hazy. The disc margins were blurred, Physiological cup filled. Colour hyper­emic. The media were clear. The discs were hyperemic, with blurred margins and lamina cribrosa not visi­ble. The veins were engorged and the arteries constricted, the A : V ratio be­ing 1:3. There was general loss of retinal markings. The macula were edematous.

General examination: -Patient ex­hibited bluish patches on both the gums see [Figure - 1] and over the trunk, having an irregular distribution see [Figure - 2].

The following investigations were carried out:­-

l. Total Red Blood Cell count--­4.1 m/Cmm.

2. Hemoglobin--13.5 Gm.%

3. Total White Blood Cell count--­9,500 /Cmm.

4. Differential white Blood cell count­-

Polymorph-59%

Lymphocytes 38%

Eosinphils-2%

Monocytes-1%

5. Erythrocytic sedimentation rate -30 mm 1st hour (Westergren).

6. Urine examination N.A.D.

7. Test for arsenic in urine (Reinsch's test)-positive.

8. V. D.R.L. test-Negative.

&

Kahn test-Negative.

Diagnosis : -

The patient was diagnosed as a case of Neuroratinitis due to arsenic poison­ing.

During his stay in the hospital the patient was treated by retrobular in­jections of Nicotinic acid (50 mg.) combined with Hyalase (20 T.R.U.) and Decadron (3 minims)--such injections being given on alternate days in each eyes.

Supportive therapy consisted of Vitamin B 1 -100mg intramuscular in­jections with Vitamin B 12 -500 mcg., Nicotinic acid tablet (25 mg) three times a day and Priscol injections

During his stay it was observed that secondary optic atrophy had set in both the eyes, more so in the left eye see [Figure - 3],[Figure - 4].

Visual status:--From initial no per­ception of light the visual acuity im­proved in the right eye to 5/60. No improvement was recorded in the left eye.

Discussion :

The case reported in this article had some unusual features. The involve­ment of both the eyes manifested as acute neuro-retinitis is rather rare. In­volvement of the optic nerve is usually manifested as a progressively develop­ing concentric constriction of the visual fields with a central depression, which is followed by pallor of the disc deve­loping into atrophy (Duke-elder ­1947).

The exact mode of affection of the ocular tissues following arsenic therapy is debatable. Since arsenic was mainly used for syphilis which also causes optic atrophy would it be correct to attribute the atrophy to the syphilitic toxin or to the poison arsenics used for its treatment. The opinion is about equally divided between the two schools of thought.

Ogden and White (1921), Zimmer­mann (1928) and Lillie (1934) favour the Sphirochetal toxin for the cause, .... whereas Grinker 1934), Stokes (1934) and Butler (1932) hold the op­posite view. Considerable support is given to the latter view by Butler's (1932) report of a case of twins suffer­ing from congenital syphilis. One of these was put on arsenic therapy and he developed optic atrophy. The other twin who was not on arsenic therapy did not develop optic atrophy.

A compromise view is offered by Moore and Woods (1924), Sloan and Woods (1936) and Lazar (1934) who suggest that an already damaged optic nerve is more susceptible to arsenic toxicity than a normal nerve. These observers, therefore, contraindicate the arsenic treatment in cases with already damaged optic nerves. Mayer (1938) on the other hand, did not agree to this statement. Fine and Barkan (1937) also, believed Tryparsamide therapy to be safe if given carefully, keeping a sharp watch upon the peri­pheral fields at a stage when the tenth injection has been reached.

Whatever be the causative factor of the ocular involvement, it is clear that arsenic administration has got to be present.

The authors, however, subscribe to the view that arsenic must be the cause of optic atrophy because the case re­ported here was not found to be suffer­ing from syphilis nor any other dis­ease that involves the optic nerve. (The initial diagnosis of Eosinophilia could not be relied upon).

It, therefore, stands to reason to assume that in the absence of syphilitic disease the ocular tissues and the nerve pathways were healthy to begin with. It was only after the arsenic treatment was instituted, that, damage to the retina and optic nerve was noted.

Moreover, by stopping the arsenic therapy and the institution of B.A.L. and vasodilators (Nicotinic acid, Pris­col with the spreading agent -- Hyalase) some recovery of the visual function in one eye was noted.[19]

Conclusion :

(1) A case of Neuro-retinitis going on to optic atrophy following arsenic therapy for suspected eosinophilia has been reported.

(2) Arsenic should be the sole cau­sative factor of nerve involve­ment in the case reported, as the patient was not suffering from any disease which is known to cause optic atrophy.

 
  References Top

1.
Butler T. H. (1932): Brit. J. Ophth. 16: 356.  Back to cited text no. 1
    
2.
Duke-elder S. (1947): Text Book of Ophthalmology p. 3020, Henry Kimp­ton, London.  Back to cited text no. 2
    
3.
Fine M. and Barkan H. (1937): Am. J. Ophth. 20: 45.  Back to cited text no. 3
    
4.
Gresser E. B. and Thomas E. W. (1942): Arch. Ophth. 28: 245.  Back to cited text no. 4
    
5.
Grinker R. R. (1934): Neurology p. 768. Charles C. Thomas. Springfield 111.  Back to cited text no. 5
    
6.
Hallum A. V. (1934): Arch. Ophth. 12: 93-98.  Back to cited text no. 6
    
7.
Hegner (1917): Quoted by Zimmermann in 19.  Back to cited text no. 7
    
8.
Kirby D. B. (1929): Arch. Ophth. 2: 661.  Back to cited text no. 8
    
9.
Lazar N. K. (1934): Arch. Ophth. 11: 240.  Back to cited text no. 9
    
10.
Lillie W. I. (1934): Tr. Am. Ophth. Soc 32: 153.  Back to cited text no. 10
    
11.
Mayer I.. L. (1938): Arch. Ophth. 19: 307.  Back to cited text no. 11
    
12.
Moore J. E. and Woods A. C. (1924): J.A.M.A. 82: 2105.  Back to cited text no. 12
    
13.
Ogden P. W. and White W.B. (1921): Am. J. Ophth. 4: 365.  Back to cited text no. 13
    
14.
Prickman Louis E. et al (1960): Am. J. Ophth. 50: 64.  Back to cited text no. 14
    
15.
Sloan L. L. and Woods A. C. (1936): Am. J. Ophth. 20: 583.  Back to cited text no. 15
    
16.
Stokes J. H. (1934): Modern Clinical Syphiliology 2nd ed. p. 1299. W. B. Saunders Co.. Philadelphia.  Back to cited text no. 16
    
17.
Tissot-Daquette (1934): Quoted by Duke-elder in 2.  Back to cited text no. 17
    
18.
Walsh F. B. (1957): Clinical Neuro-­ophthalmology 2nd ed. p. 553. The William and Wilkinson Co. Baltimore.  Back to cited text no. 18
    
19.
Zimmerman E. L. (1928): Arch. Ophth. 57: 509.  Back to cited text no. 19
    


    Figures

  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]



 

Top
 
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
Case Report
References
Article Figures

 Article Access Statistics
    Viewed1145    
    Printed29    
    Emailed0    
    PDF Downloaded0    
    Comments [Add]    

Recommend this journal