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Aust. J. Optom.

(1983); 66,( I ) : 3-12

Toxic Cataract
P.G.Swann* and J.F. Elliott?
Department of Optometry, Queensland Institute of Technology

ABSTRACT A host of ocular adverse reactions may adverse drug reactions, the mechanisms of toxicity and
result from the use of systemic medications. Included the variables concerned in the productions of such side
in these reactions is that of the crystalline lens effects.
known as toxic cataract. This paper will consider A n early classification recognised overdose,
this response with special reference to lens changes intolerance, side effects, secondary effects, idio-
resulting from the use of steroids and certain tran- syncrasy and hypersensitivity.75When the mechanism
quillizers. of toxicity is known, these reactions can be divided
Keywords: ocular adverse reactions, toxic cataract, into:78
steroid cataract, chlorpromazine cataract. 1. Dose related: -
(a) side effects - unavoidable pharmacological
Introduction effect.
In 1973, Davidsonlstated that of the 28,000 cases of (b) secondary - indirect consequence of drug
drug adverse reactions reported to the Committee on action. Predictable - dilution may reduce or
Safety of Drugs since its establishment in 1963, 1,000 abolish reaction.
reports were made in reference to the eye. Of these, 2. Unrelated to dose:-
about 5O/n concerned the crystalline lens and the onset (a) allergy
of toxic cataract or lens deposits. Davidson also noted (b) idiosyncrasy - genetic predisposition
that only a very small proportion of adverse events 3. Unknown
would be reported using such. a voluntary system - 4. Teratogenic
5 . Interactions.
perhaps as few as lo/n.
The cataractogenic nature of certain substances, Furthermore, the variables involved in the produc-
whether medicinal or otherwise has been known for tion of a side effect should be defined. They
many years.2" Good examples are the slimming agent include"?-
dinitrophenol, the insecticide paradichlorobenzene 1. The nature of the drug
and the salts of certain metals such as thallium. Many 2. The amount consumed
such preparations have now been discontinued. 3. The route of administration
However, a considerable number of potentially 4. The patient's general health, the condition being
cataract-producing systemic drugs are available and treated
some such as the cortico-steriods and the 5 . Individual idiosyncrasy
phenothiazines are regularly prescribed. 6. Other substances which may potentiate side effects
Table 1 lists drugs where evidence for catarac- 7. Previous exposure to the drug.
togenity is strong; and Table 2, those drugs where Rawlins and Thompson7shave simplified matters by
reports have been more isolated and less compelling. dividing adverse drug reactions into those that arise
In addition, a few preparations have been listed as hav- from the normal pharmacological action of a drug, and
ing a teratogenic effect on the lens, either before term those that represent a totally abnormal and novel
or via lactation. Table 3 lists these drugs. response; that is, type A and type B reactions.
A n adverse reaction to a drug can be defined as a
response that is noxious and unintended, and occurs at Type A Reactions
dosages used in man for prophylaxis, diagnosis or Resulting from an exaggerated, but otherwise nor-
therapy, excluding failure to accomplish the desired mal pharmacological action of a drug given in the usual
purpose. Many attempts have been made to classify therapeutic doses, Type A reactions are frequently pre-
* Senior Lecturer- dictable on the basis of a drug's known pharmacology.
t Optometrist, Brisbane They are usually dose dependent.

3
Generic Name Brand Name

CORTICO
-STEROIDS16-25
Aldosterone
Betamethasone
Cortisone
Aldocorten
Celestone
Austracort
hti-Inflammatory Posterior
Subcapsular
Cataracts
' Increased
LOP.:
Myopic shift :
Desoxycorticosterone Cortiron Exophthalmos:
Dexamethasone Dexasone Extraocular
Fludrocortisone Florinef muscle paresis:
Fluorometholone F.M.L. Liquifitm Field defects:
Fluprednisolone Alphadrol Retinal oedema
Hydrocortisone Hycor and
Medrysone H.M.S. Liquifii haemorrhages:
Methylprednisolone Medrol conjunctival
Paramethasone Metilar oedema and
Prednisolone Prelone hemorrhages.
Prednisone Presone
Triamcinolone Aristocort
PHENOTHIMINES
Chlorpromazine26-38 Largactil Antipsychotic, Stellate anterior Granules in cornea:
Trifluoperazine34-35 Stelazine (tranquillizer) capsular and Field defects:
subcapsulargranules. Ocular melanosis:
moridazine36-37 Mellaril Polar cataract Pigmentary retinopathy :
Prochlorperazine73 Stemetil following high dosages. Optic atrophy:
Fluphenazine34 Modecate Oculomotor palsies:
Methotrimeprazine34 Veractil
I I
PIPERAZINE
DERIVATIVE
1+Bis - Diphenazine; Antipsychotic
1
@henylisopropyl)- Quietidin (trallquillizer) and anterior radial of hair and eyebrows.
piperazine9.39
~ o p ~ i n o1340,82983
Ill Zyloprim
capsular changes. reactions.
Anterior subcapsular

Eyelid and conjunctival


opacities reactions; Retinal
haemorrhages; Decreased
viaion.
Table 1: Cataractogenic systemic drugs.

Generic Name Brand Name Drug Action cataract Type Other Ocular Changes

BUTYROPHENONES
Haloperid0113e43 Serenace Antipsychotic. Capsular cataracts. Pupil and accommodation
Trifluperidol Triperidol (tranquillizer) Rapid progression. anomalies: Eyelid and
conjunctival reactions:
Visual hallucinations.
THIOXANTHENES
ChlorprothixenegJ3 Taractan Lens deposits beneath Retinal pigmentary
anterior capsule: changes: Pupil and
Thiothixene Navane Fine lenticular accommodation anomaliis:
pigmentation. Keratitis.
Chloroquin Anti-malatial Posterior axial Retinopathy: Corneal
subcapsular flakes. opacities; Optic atrophy;
Hydr oxychloroquine Plaquenil Brown anterior surface Field defects.
flakes.
Anorex Anorexiant Posterior subcapsular Pupil, accommodation and
Duromine opacities convergence anomalies.
Clomid Ovulatory Agent Posterior subcapsular Loss of central vision;
cataracts scintillatinn scotoma.
Hyperstat Antihypertensive Information unavailable Lacrimation; Lid and
conjunctival reactions;
Decreased vision.
Table 2: Possibly cataractogenic systemic drugs. * Continued Overleaf
4 Aust. J. Optom,, 66.1: January 1983
* Continued
Generic Name Brand Name Drug Action Cataract Type Other ocular ChulgeIl

Ibuprofen1 3 4 Brufen Analgesic


Field defects.
Chelating agent Possibly anterior and Eyelid and conjunctival
posterior subcapsular reactions.
chanees.
Carbromal6O C.N.S. depressant, Opacities throughout Nystagmus; Pupil
(sedation) the entire lens. anomalies:Optic
(reversible)? neuritis.
~it0tanel3 Lysodren Posterior subcapsular Eyelid and conjunctival
Actinomycin D61 Dactinomycin opacities. reactions; Retinal
Chromomycin A3 Toyomycin haemorrhages;
Mitomycin C Mutamycin Decreased vision.
Vincristine oncovin
Aurothioglucosel3~62 Solganal Anti-rheumatic, Reddish-brown anterior Gold deposits in the
Aurothiomalate Myochrysine (Gold compounds) axial and sutural conjunctiva and cornea;
subcapsular deposits. Eyelid and conjunctival
allergic reactions.
Qomac1an7Q DeWYl Antipsychotic, White or brown stellate Possible photosensitivity.
(tranquillizer) anterior capsular Corneal granules.
deposits; possibly
reversible.
DiphenylhydrantoinB1 Dilantin Anticonvulsant Posterior subcapsular Nystagmus; Diplopia;
changes. Blurred vision.

Table 2: Possibly cataractogenic systemic drugs.

Type B Reactions rheumatoid arthritis, asthma and systemic lupus


These reactions are unexpected from the known erythematosus. Spaeth and Von Sallmann analysed
pharmacological actions of a drug when given in the reports of 693 patients having such conditions, and
usual therapeutic doses. They are mostly unpredicta- being treated with steroids, and found that 21'% showed
ble. Unlike Type A reactions, their incidence and mor- posterior subcapsular cataract. This compares to an
bidity are usually low, and their mortality may be high. incidence of about 0.2'%1in the overall population. The
Therapy may have to be withdrawn. findings of other studies are pfesented in Table 4.
The majority of drug-induced crystalline lens Drug therapy, whethqr steroid or not, is by no
changes are Type A, with a few examples ofType B74 means the only way of causing similar lenticular
changes. They may be observed as:
Corticosteroids
1. Senile cupulliform punctate opacities, occurring
The occurrence of toxic cataractous changes follow- spontaneously in the geriatric eye,
ing the administration of corticosteroids was first 2. Complicated or secondary changes following some
reported by Black rt a15 in 1960. Many subsequent longstanding intra-ocular disease such as uveitis or
reports have confirmed this original observation. The retinitis pigmentosa, (Figure 1 ).
opacification is initially seen in the axial region of the 3 . Congenital posterior polar cataract, probably due to
posterior subcapsular cortex, and may progress malabsorption of the hyaloid system, (Figure 2 ) .
towards the lens equator at this level. 4. Radiation induced cataract, f r o m prolonged
Many diseases may require systemic or topical exposure to infra-red wavelengths.
steriod therapy. Examples of t h e f o r m e r a r e 5 . The less common form of dermatologic atopic
cataract occurring at the posterior pole of the lens in
the subcapsular region.22
Name Action

I Radiomimetic
tetracycline^^^-^
Sulphonamides64-67 I
No. of
Datients
693
Percentage exhibiting lens changes

21 (Spaeth and Von Sallmann, cited by


I
Debendox64-66 Patterson5)
Antiemetic
Cyclizine69 I 39 5 1 (Skaka and Rchalno)
Carbimazole71 I Anti-thyroid 1 86
62
33 (Donshik et al23)
58 ( A d h i et al24)
~~ ~ ~~

Table 3: Drugs where a teratogenic cataractous effect has been


suggested. Table 4: Incidence of corticosteroid induced lens changes.

Aust. J. Optom.. 66.1: January 1983 5


Figure 1: Complicated or secondary cataract. Figure 2: Congenital posterior polar cataract.

6. A type of hue diabetic cataract manifesting as a therapys, it is widely believed that children are more
posterior subcapsular opacity and frequently show- susceptible than adults to cataract formation following
ing fine granular radial striae extending from the corticosteroid administration.
equatorial regions into the main opacity.80 The role of individual susceptibility has been
Careful investigation of the patient’s ocular and explored by Skalka & Prchal.2OTheir study confirmed a
general health as well as occupational factors should correlation between the incidence of posterior subcap-
make the diagnosis certain. sular catpact and the administration of corticosteroids,
Dosage and Susceptibility but failed to find a statistically significant relationship
The relevant literature discloses disagreement on between lens opacities and total dose, weekly dose,
the relationship between corticosteroid lenticular duration of dose or the age of the patient. They suggest
changes and total dose, dosage intensity and the dura- that the most important factor may be an individual
tion of administration of the medication. susceptibility to the side-effect of corticosteroids, and
Early reports have suggested that 75% of patients propose abandonment of the concept of a ‘safe dose’.
receiving Prednisone in excess of 15 mg/day would Cataracis h a v e been reported following t h e
develop posterior subcapsular lens opacitiess, whereas administration of corticosteroids via an aerosol spray21,
dosages of less than 10 mg/day of Prednisone o r its and the association between topically applied cor-
equivalent were unlikely to excite the formation of ticosteroids to the eye and cataracts is well known. 17.19.23
cataract.’* Similarly, patients treated for less than one Posterior subcapsular cataracts were n o t e d by
year, or who were receiving intermittent therapy, were Donshik, et aP3, in 28 out of 86 eyes subjected to topi-
held to be less at risk. However Loredo, ef UP,have cal corticosteroids following keratoplasty for
reported cataracts occurring in children who received keratoconus. The development of opacities was signifi-
corticosteroids for periods ranging from 3 to 10 cantly related to total cumulative dose and the total
months. The concept of a ‘safe dose’ or ‘boundary period over which steroids were administered. Cases
figure’ has been suggesteds, and a systemically where unilateral topical steroids have produced
administered Prednisone equivalent of 3.5 gm in one cataract in the treated eye only, have also been
year has been considered to approximate such a figure. reported. 5
The underlying disease may have a bearing on the Corticosteroid induced glaucoma and cataracts have
incidence of lens changes. For example, some authors been reported in patients for whom the drug was
believe that arthritics are m o r e a t risk than prescribed to reduce irritation produced by contact lens
asthmatics.79 Whilst i t can be contended that wear.17 Individuals with a high degree of myopia and a
asthmatics are younger and receive a less concentrated family history of glaucoma have an increased suscep-

6 Aust. J. Optom., 66.1 :January 1983


tibility to this condition. Also, young myopes con-
stitute a considerable number of contact lens wearers.
Appearance
The process commences in the axial region of the
posterior subcapsular cortex. An irregular iridescence
is seen in this area and the opacification usually spreads
both into the cortex of the lens and beneath the
posterior capsule. Frequently, the outlines of the
opacity are clear. Fine yellowish-white opacities and
vacuoles are seenlz.3Js (Figures 3 & 4). The cataractous
appearance is the same whether it is associated with the
use of systemic or topical steroids.25
Greiner and Chylachzs, in a histopathological study
of steroid cataracts noted that they and senile posterior
subcapsular cataractous changes corresponded closely
in late mature stages. The changes included a swelling
of superficial lens fibres followed by liquefaction of Figure4: Steroid cataractous changes seen with a narrow slit sec-
subcapsular cortical fibres, forming a region beneath tion.
which was a further zone of swollen fibres. At earlier
stages of development, a major difference existed in
the extent of anatomical damage. In steroid cataract the
damage was more localised and limited to the polar
region, whereas in comparable senile posterior subcap- E.F. SYSTEMIC LUPUS ERYTHEMATOSUS
sular cataract the affected area was more diffuse and
extensive. 16.3.72
The exact mechanism whereby these changes are R L
produced is illusive.5 It has been suggested that both
anterior and posterior surfaces undergo a change in
lens fibre permeability that tends to result in altered
cation and water distribution. The anterior surface,
though, has the ability to correct potential imbalances
due to its active epithelium, and thus cell hydration
and vacuole formation are only able to continue at the Prednisone up to 40 mg/day
posterior surface.
28.7.72

Prednisone up to 40 mg/day

1.9182

No regular Prednisone since January 1973.


Drug occasionally taken for very short periods when
:ondition active.
Figure 3: Steroid cataract following administration of prednisone Figure 5: Regression of steroid lens changes following removal of
-
for asthma, retro-illumination view. regular prednisone medication.

Awt. J. Optom, 66.1: January 1983 7


Progression and Regression ly exacerbated by sunlight where dazzle and glare
Lens changes may remain stationary in the early effects are pronounced.
stages provided dose levels are minimal.78 Should Further difficulties may be produced by changes in
progression occur, withdrawal of the medication may refraction, and in particular the development of a tran-
stabilise the process23, although continued advance- sient myopia.3J6 An example is the refractive status of
ment has been noted in such situations.sRegression of the patient depicted in Figure 6, wherein a rapid and
the opacities has been observed.s.21 A patient seen by continuous myopic shift of about 5 dioptres occurred
one of us (P.G.S.), has also appeared to demonstrate a from the time lens changes were first noted to the date
regression (Figure 5 ) . Diagrams illustrating the of cataract extraction. During this period, the base line
posterior subcapsular opacities and subsequent visual intake of Prednisone was 15 mg/day, rising on many
acuities are shown for 1972.77 Regular corticosteroids occasions to 30 mg/day when asthma attacks were
were discontinued 9 years ago, and the current state of severe.
the opacities is given. The patient suffers no subjective Tranquillizers
problems other than a very slight dazzle on particularly A drug which is capable of inducing a state of calm
bright sunny days. without hypnosis is called a tranquillizer.74 Tran-
Visual.Symptoms quillizers may be classified into two groups depending
Any posterior polar lens change may cause a con- on whether their main use is directed towards the treat-
siderable disturbance of vision due to its proximity to ment of psychoses such as schizophrenia - the major
the nodal point, and its axial position. The effect on rranquillizers, or whether they are used to treat anxiety
visual acuity is minimal in the early stages23, and vision . states - the minor tranquilizers. The former have been
may be quite good even in established cases. Most of implicated in the production of toxic lenticular changes
the patients described by Adhikary et aP4, for example, which initially are deposits in nature, and later may
had a visual acuity better than 6/12. become frank cataractous opacities.
The degree to which a patient is debilitated by the Broadly, the major tranquillizers include the
cataract depends on many occupational, recreational butyrophenones, the phenothiazines and the thiox-
and environmental factors. Problems ensue in situa- a n t h e n e s . E v i d e n c e i m p l i c a t i n g t h e
tions that initiate pupil constriction, and are particular- butyrophenones13.43 and the thioxanthenes9J’ in the

J.O.Asthma: Prednisone, up to-30 mg/day first commenced 1978.

r3D

+ 2D

ilD

Plam

-ID

-20

- 3D

1974 1978 : May : May : Aug : Aug : Sept : Feb : March : June : July
1380 1981 1981 i 1981 I 1981 i 1982 1982 i 1982 i 1982 i
*
%2

Figure 6: Development of a myopic shift in refraction during prednisone administration.

8 Aust. J. Optom.. 66.1: January 1983


onset of lenticular anomalies is far less compelling than
that for the phenothiazines26-38. Other tranquillizers D.H.
such as Quietidin9.39, (a piperazine derivative), and R L
Clomacran70, (a drug related to the phenothiazines),
have also been accused of having a toxic lenticular side
effect.
It is the phenothiazines however, which have
attracted most attention since Greiner and Berry’s26
original report on the oculo-cutaneous toxicity of
chlorpromazine in 1964. They described ocular and
dermatologic complications occurring in 70 female
patients who had been receiving chlorpromazine for at
least 3 to 5 years in dosages averaging from 500 to 1500 J.G.
mglday.
In general terms, the lens changes mainfest as tiny
brown punctate deposits in the anterior lens which may
take on a stellate configuration. Concomitant pigmen-
tation of the cornea, conjunctiva, retina and skin may
occur. The reaction is probably one of photosen-
sitivity. 5
Other situations in which similar deposits may occur
in or on the anterior lens include:
1. Stellate pigment dust or epicapsular stars - the L.
most common and rudimentary form of persis-
tence of the pupillary membrane,
2. Axial pigmentation of the crystalline lens, -
manifesting as stellate shaped zones of tiny brown
dots in and under the anterior capsule, seen com-
monly in the elderly patient and rarely in patients
under 30 years of age, (Figure 7).
3. Fine brownish deposits on the anterior capsule, -
implicated as a side effect of the drug chloro- Central anterior polar cataract in left eye.
quine 47.50 Figure 8: Appearance of chlorpromazine lens changes seen in the
4. Minute reddish brown granules in and under the right and left eyes of three institutionalized patients.
anterior capsule, possibly stellate and resulting
from treatment with gold compounds - ocular
chrysiasis 13-62, Dosage and Susceptibility
Again a thorough case history and slit-lamp Various studies have revealed the incidence of lens
examination should present no problems for changes to be from 27 to 76%.5 An example is that by
accurate diagnosis. Mathalone27.28 who showed that of patients who were
receiving more than 300mg of chlorpromazine daily for
3 years or more, 36% manifested lens changes and 17%
corneal changes. The usual threshold for lenticular,
corneal and conjunctival toxic effects is a cumulative
dose of 500 to 1000 gm. Patients receiving a total dose
of 2500gm may show a 9Oo/n evidence of lens involve-
ment.5
Some degree of individual susceptibility may be
involved, and some patients may be more resistant
than others. Mathalone28 noted several subjects who
had received fairly large doses but showed no sign of
ocular toxicity, and one who manifested slight lens
changes after less than one year’s treatment.
Evidence relating to other phenothiazines is some-
what inconclusive. Most reported treatment regimens
have had chlorpromazine playing a major role. Stellate
lens changes have been recorded after 600 to 800 mg of
thioridazine per day for 44 months prior to examina-
tion.37 Also, trifluoperazine has been implicatedw.35 as
Figure 7: Axial pigmentation of the lens. well as methotrimeprazine and fluphenazine35. Ocular

Aust. J. Optom., 66.1: January 1983 9


A phototoxic mechanism appears to be responsible
for the formation of these changes.5 Chlorpromazine is
a phototoxic compound, and therefore the potential
exists for it to cause cellular damage after light
exposute.J*I t has been suggested that chlorpromazine,
as a photo-sensitizing agent, will denature protein
when exposed to sunlight, and deposits and later
opacities are formed in the axial, anterior capsular and
subcapsular areas. Deluise & Flynn33 described a
patient who showed chlorpromazine ocular toxicity
following ingestion of 800 mg/day for 10 years. The
patient also manifested a congenital right ptosis, and
the anterior segment changes were far less pronounced
in that eye.
Progression and Regression
If patients are maintained on very high dosage levels
of chlorpromazine then the lens changes may be
progressive. Deposits give way to obvious opacities,
and reduplicated stellate configurations may occur.
Figure 9: Stellate chlorpromazine deposits seen with direct focal Similarly, an anterior polar cataract can develop.
illumination with a wide slit. The cataractous process may stabilise if dose levels
become moderate. 31 Some have claimed an accelerated
reduction of deposits with chelating agents.5 Many
toxicity is probably a potential hazard of prolonged authors have observed a regression in lens, corneal,
therapy with all phenothiazines. 34 conjunctival, retinal and skin changes29J0J2J7,although
Appearance it is unlikely that the lens opacities will ever totally dis-
appear. Phenothiazines combine with ocular and der-
See Figures 8, 9, 10 and 11. Lens changes are mal pigment and are only slowly released. This slow
bilateral, axial, and initially lie within the anterior cap- release has in part been given as the reason why toxic
sule. They have an overall disciform shape in the early effects may seem to progress after the drug is discon-
stages, and are yellowish white in colour. As the condi- tinuedl3, or why a regression process appears
tion progresses, discrete brown granules assume a stel- protracted.
late pattern, which may invade the anterior cortex, and
reduplication can occur. Large prolonged doses may Visual Symptoms
lead to the formation of white anterior polar Frequently, visual acuity is minimally affected.28J.32
opacities.3.79 Concurrent pigmentation of the cornea, Twenty-three of Siddall's37 78 patients had a corrected
conjunctiva, retina and skin may be observed. visual acuity of less than 6/7.5, and 17 of those subjects

Figure 10: The same changes as figure 9 observed with the fundus Figure 11: Anterior polar cataract following long term, high dosage
camera. chlorpromazineand trifluoperazine medication.

10 Aust. J. Optom, 66.1:January 1983


ranged between 619 and 6/24. One patient had an case of steroids, a topical application may hold the
acuity of 61120 following massive d o s e s of same risks. Unfortunately, the usefulness of these
chlorpromazine. Retinal pigmentation accounted for drugs may overide the possible hazard. Nevertheless,
reduced acuity in 4 patients, and one of those was blind regular ophthalmic examinations are mandatory for
from receiving thioridazine in huge quantities. these patients, and reduce the risk of ocular toxicity
Other potential vision problems are a paralysis of progressing without detection during long term
accommodation, night blindness, disturbances of col- therapy. The Optometrist must always be aware of any
our vision and visual field anomalies. patient's medication regimen, and be in a position to
inform the physician of the onset of side effect.
Summary
I t would seem that two groups of systemic medica-
tions, namely t h e corticosteriods a n d t h e Acknowledgements: We thank David Cockburn for the photograph
phenothiazines, are potentially cataractogenic. In the of the complicated cataract. Julie Halliday drew Figure 6.

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