Mydriasis and glaucoma: exploding the myth.

A systematic review
R. J. Pandit* and R. Taylor

Departments of *Ophthalmology and Medicine,
Royal Victoria Inrmary, Newcastle upon Tyne, UK
Accepted 3 August 2000
Abstract
Aims To investigate the risk of inducing acute glaucoma following mydriasis.
Methods Systematic review of published research 19331999.
Results The risk of inducing acute glaucoma following mydriasis with
tropicamide alone is close to zero, no case being identied. The risk with long-
acting or combined agents is between 1 in 3380 and 1 in 20 000. The presence
of chronic glaucoma constitutes no additional risk.
Conclusions Mydriasis with tropicamide alone is safe even in people with
chronic glaucoma. It should be advised in all patients when thorough retinal
examination is indicated.
Diabet. Med. 17, 693699 (2000)
Keywords glaucoma, intraocular pressure, mydriasis, pilocarpine,
tropicamide
Abbreviations IOP, intraocular pressure

reason for not dilating pupils routinely [11]. In particular,

Introduction
The necessity to dilate the pupil to permit adequate
fundoscopy was recognized in the 19th century following
the invention of the ophthalmoscope [1,2]. Today,
although mydriatic eye drops are used routinely by
ophthalmologists whenever fundoscopy is indicated, they
remain seldom used by physicians [3]. In general medical
practice, the commonest indication for pupil dilation is in
screening for diabetic retinopathy, where it increases the
sensitivity of screening by over 50% [47]. The health
gains of comprehensive screening for diabetic retinopathy
are high. Thus, proper screening followed by early
treatment of sight-threatening disease has been shown to
reduce new blindness as the result of diabetes by more than
a third [8].
The possibility of inducing acute glaucoma by mydriasis
has also been recognized for over a century [9,10] and is
often cited by diabetologists and general physicians as a
Correspondence to: Professor Roy Taylor, Diabetes Unit, Claremont Wing,
Royal Victoria Inrmary, Newcastle upon Tyne NE1 4LP, UK.
E-mail: roy.taylor@ncl.ac.uk
patients who give a history of glaucoma of any kind are
usually deprived of diagnostic mydriasis on account of this
concern. Thus, it is the policy of most medical and diabetes
units not to dilate the pupils of these patients, and this
advice is reiterated in many authoritative texts [1217].
This practice is not evidence-based and denies many people
effective examination.
This article will review the published evidence on the risk
of inducing acute glaucoma following mydriasis.
Additionally, the common practice of using pilocarpine
to reverse mydriasis is questioned.
Methods
Medline and Embase searches on `mydriasis', `intraocular
pressure', and `glaucoma' identied 26 original studies on the
subject of intraocular pressure changes or acute glaucoma
following mydriasis. Isolated case reports were excluded. Eight
studies were found to have insufcient data or inappropriate
design for the purpose of this review (lack of complete
ascertainment). All reference lists of the identied papers were
examined, and a further 10 studies were identied. The 28

2000 Diabetes UK. Diabetic Medicine, 17, 693699 693

 694 Mydriasis and glaucoma: exploding the myth R. J. Pandit & R. Taylor

Table 1 Key features of chronic and acute glaucoma

Chronic glaucoma* Acute glaucoma*

(primary open angle glaucoma) (primary acute angle closure glaucoma)

Prevalence 12% 0.040.2%

(accounts for ~ 95% of all glaucoma)

Typical age onset > 40 years > 50 years (usually elderly)

Sex F=M F > M (5 : 1)

Family history +

Racial predilection Afro-Caribbeans Eskimos

SE Asians
Chinese

Refractive error Hypermetropia

Presentation Bilateral Unilateral

(often asymmetric onset and progression) (fellow eye at high risk)

Onset Insidious Acute

Progression Slow Rapid

(blindness years to decades) (blindness hours to days)

Symptoms None Pain

(until advanced) headache
photophobia
nausea
vomiting
reduced vision
coloured haloes

External signs None Injection

tenderness
corneal clouding
mid-dilated and poorly reacting pupil

*Terminology used in this review; Caucasians over the age 40; insufcient data; possible weak association with myopia.

studies (26 8 + 10) were categorized into studies on the results
of mydriasis in 1 the general population (six studies), 2 people
already known to have chronic glaucoma (13 studies), 3 eyes
following iridectomy for acute glaucoma (three studies), and 4
untreated fellow eyes of people who had suffered acute
glaucoma in one eye (six studies). Each group is discussed in
turn.
drainage angle. Acute glaucoma is uncommon and is a
very different disease. It occurs in `anatomically predis-
posed eyes' as a result of closure of the angle by peripheral
iris. The precipitation of angle closure in these eyes relates
to the development of a relative pupillary block to normal
aqueous ow [18].

Chronic and acute glaucoma (Table 1)
In this review, the terms chronic and acute glaucoma are
used to refer specically to primary open angle and primary
acute angle closure glaucoma, respectively. Confusion
about these conditions may lead to reluctance to dilate the
pupils of glaucomatous eyes. Chronic glaucoma is com-
mon and occurs in `anatomically normal eyes'. The raised
intraocular pressure (IOP) is attributed to increased
resistance to the outow of aqueous humour in a
macroscopically normal and open anterior chamber
Risk of acute glaucoma following mydriasis
Studies in the general population (Table 2)
Two large retrospective surveys of ophthalmology prac-
tices identied cases of acute glaucoma following mydria-
sis and estimated the total number of mydriatic
examinations performed during the same period [19,20].
They both placed the risk at about 1 in 20 000. In these
surveys, mydriasis was performed using long-acting agents
(atropine or homatropine) and combined agents (tropica-

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 Review 695

Table 2 Incidence of acute glaucoma following mydriasis in the general population

Survey Mydriatic agent Number Acute glaucoma (n) Incidence

Abraham 1933 [19] Atropine and homatropine 535 500* 29 1 in 18 400

Talks et al. 1993 [20] Tropicamide 1% plus phenylephrine 10% 40 000* 2 1 in 20 000
Phenylephrine 2.5% 546 0 0
Phenylephrine 10% 159 0 0

Yolton et al. 1980 [21] Tropicamide 0.5% 614 0 0

Tropicamide 1% 537 0 0
Cyclopentolate 0.5% 73 0 0
Cyclopentolate 1% 58 0 0
Phenylephrine 2.5% 2166 0 0
Tropicamide 0.5% 1133 0 0

Applebaum & Jaanus 1983 [22] Tropicamide 1% 1650 0 0

Cyclopentolate 0.5% 20 0 0
Cyclopentolate 1% 116 0 0
Hydroxyamphetamine 1% 22 0 0
Tropicamide 1% plus phenylephrine 2.5% 5270 0 0

Patel et al. 1995 [24] Tropicamide 0.5% 38 0 0

Wolfs et al. 1997 [23] Tropicamide 0.5% plus phenylephrine 5% 6760 2 1 in 3380

Total All agents 594 662 33 1 in 18 020

Tropicamide alone 3972 0 0

*Estimated.

mide plus phenylephrine), respectively. Two prospective
surveys in optometry practices did not record a single case
of angle closure following mydriasis with a wide variety of
agents in over 7000 people [21,22].
More recently there have been two cross-sectional
population based studies addressing this risk. In the
Rotterdam study, two of 6760 people developed a
unilateral acute glaucoma after mydriasis with the
combination of tropicamide and phenylephrine [23]. This
placed the risk at 1 in 3380. The prevalence of narrow
angles detected by the Van Herick slit-lamp method was
2.2% (n = 149), and only one of the two cases of acute
glaucoma fell into this category. Thus, a narrow angle as
detected by this method correlated poorly with the
development acute glaucoma following mydriasis. In this
study, its positive predictive value was 0.67% (1/149).
In the Baltimore survey, trained retinal screeners
performed the initial assessment of 5308 people [24].
They dilated the pupils of 4870 people using a combination
of tropicamide and phenylephrine and no-one developed
acute glaucoma. Of these, 1332 were referred for denitive
ophthalmic examination because of abnormal ocular
ndings. Additionally, the 438 subjects who were not
dilated by screeners for a variety of reasons were also
referred (53084870). These included those on treatment
for glaucoma, and those in whom a shallow anterior
chamber was suspected on oblique penlight examination.
Only 38 of the 1770 patients (1332 + 438) were judged to
have occludable angles by gonioscopy, and the remainder
underwent uneventful mydriasis. Twenty-eight of these 38
were safely dilated with tropicamide alone, and in the
remaining 10, a laser iridotomy was performed prior to
uneventful mydriasis. This made the interpretation of risk
difcult. It cannot be assumed that these 10 patients would
have developed acute glaucoma if they had been dilated
prior to iridotomy. Indeed, there is evidence indicating that
a narrow angle is, in isolation, a poor predictor of the
likelihood of mydriatic-induced acute glaucoma as was the
case in the Rotterdam study [23,2527]. As it stands, acute
glaucoma did not occur following mydriasis in the
Baltimore survey.
Studies on people with chronic glaucoma (Table 3)
Several studies have shown that IOP may rise transiently
following mydriasis in some eyes with chronic glaucoma by
mechanisms not involving angle closure [2841]. To put
into context the degree of IOP rise represented in such
studies, normal IOP is accepted as 1121 mmHg (popula-
tion mean 16 mmHg 6 2SD), and about 30% of normal
eyes show a diurnal uctuation of IOP of up to 5 mmHg.
Most patients with chronic glaucoma have an IOP of 23
40 mmHg at presentation, whereas the IOP in acute
glaucoma tends to be much higher (usually > 50 mmHg).

2000 Diabetes UK. Diabetic Medicine, 17, 693699

 696 Mydriasis and glaucoma: exploding the myth R. J. Pandit & R. Taylor

Table 3 Incidence of acute glaucoma following mydriasis in people with chronic glaucoma

Miotic Transient DIOP 6 SD Acute

Study Mydriatic agent therapy Number IOP riseae (n) (mmHg) glaucoma (n)

Kroneld et al. 1943 [32] Homatropine 5% No 22 7e NS 0

Hydroxyamphetamine 2% No 22 2e NS 0
Homatropine 5% plus No 18 10e NS 0
hydroxyamphetamine 2%

Lee 1958 [33] Phenylephrine 10% NS 6 4e +12.8 6 11.0 0

Adrenaline 1% NS 10 1e +2.8 6 4.7 0

Becker et al. 1959 [34] Phenylephrine 10% Yes 16 0a 1.9 6 1.7 0

Schimek & Lieberman 1961 [35] Cyclopentolate 1% Yes 17 9e +6.4 6 5.7 0

Phenylephrine 10% Yes 17 0e +0.5 6 3.8 0

Christensen & Pearce 1963 [36] Homatropine 5% No 35 24a +3.0 6 2.5 0

Harris 1968 [28] Cyclopentolate 1% Yes 40 9c NS 0

Atropine 1% Yes 11 11c NS 0
Homatropine 5% Yes 11 11c NS 0
Scopolamine 0.25% Yes 11 7c NS 0
Eucatropine 5% Yes 11 0c NS 0
Cyclopentolate 0.2% Yes 11 0c NS 0
Tropicamide 0.5% Yes 11 0c NS 0
Phenylephrine 10% Yes 11 0c NS 0

Hill 1968 [41] Phenylephrine 10% Yes 30 6a NS 0

Lazenby et al. 1968 [29] Cyclopentolate 1% Yes 28 14b NS 0

Harris & Galin 1969 [40] Cyclopentolate 1% No 38 9c NS 0

Yes 69 30c NS 0

Portney & Purcell 1975 [31] Tropicamide 1% No 25 0d 0 6 2.8 0

Yes 25 4d +3.5 6 3.5 0

Valle 1976 [37,38] Cyclopentolate 1% No 196 17e +2.5 6 3.1 0

No 235f 4e +0.4 6 2.5 0

Shaw and Lewis 1986 [30] Tropicamide 1% plus No 58 13b NS 0

phenylephrine 2.5% Yes 58 24b NS 0
(+2.9 6 5.4 overall)

Campeas et al. 1999 [39] Tropicamide 1% plus NS 33 0d 0.4 6 1.5 0

phenylephrine 2.5%

Total All agents Yes/no or NS 1075 216ae 0

Yes 377 125ae 0
No 649 86ae 0
Tropicamide alone Yes/no or NS 61 4c,d 0
Yes 36 4c,d 0
No 25 0c 0

NS, not stated.

Cut-offs for intraocular pressure (IOP) rise used in studies: a1 mmHg, b5 mmHg, c6 mmHg, d7 mmHg, e8 mmHg. fSuspected chronic open angle
glaucoma patients.

Harris studied 100 healthy subjects and 40 with chronic in two (2%) and nine (23%) eyes, respectively. The IOP
glaucoma and used fellow eyes as controls [28]. A transient rise was generally detectable at 30 min, was maximal at
response (> 6 mmHg IOP rise) to cyclopentolate occurred 90120 min, and had subsided by 46 h. Acute glaucoma

2000 Diabetes UK. Diabetic Medicine, 17, 693699


did not occur, and gonioscopy conrmed that angles
remained open throughout the period of study. In a
substudy of the 11 responders (2 + 9), he found that they
all responded to other long-acting mydriatics but not to the
short-acting agents such as tropicamide.
Several points emerge from this and the other
studies detailed in Table 3. Firstly, and most impor-
tantly, acute glaucoma does not occur following
mydriasis in eyes with chronic open angle glaucoma.
Not a single case is documented in the 13 studies
involving over 1000 patients.
Secondly, there is great variation in the IOP response
both between and within the studies. For example,
following mydriasis with cyclopentolate, Lazenby and
colleagues [29] found a transient IOP rise in 14/28 of eyes
(50%) compared to 9/40 (23%) in the study by Harris [28].
In the study by Shaw and Lewis [30] of 116 eyes, IOP
rose >5 mmHg in 37 eyes (32%), actually fell in 34 eyes
(29%), and remained unchanged or rose < 5 mmHg in 45
eyes (38%) after mydriasis with the combination of
tropicamide and phenylephrine. The bi-directional nature
of the IOP response within a study population is
documented by others, and the variation in its magnitude
is reected by high standard deviations about the mean
[3139]. Harris has also noted that the IOP response to a
particular agent is not consistently reproducible in the
same patient or eye [28].
Thirdly, it appears that miotic therapy for chronic
glaucoma is associated with a transient IOP rise when long-
acting or combined mydriatics are used. Thus, the
percentage of responders falls from about 40 to 20%
when miotics are discontinued prior to mydriasis with
these agents [30,40]. This association is weaker when
tropicamide is used alone. Thus, none of the miotic treated
eyes in Harris' series responded to tropicamide [28]
compared to only 16% (4/25) in Portney and Purcell's
series [31]. It should be noted that with the advent of better
tolerated agents, miotics are no longer used commonly in
the treatment of chronic glaucoma.
The occurrence of a transient IOP rise is less frequent
when tropicamide is used alone. Thus, the combined data
give an overall occurrence of 20% (216/1075) compared to
7% (4/61) when tropicamide is used alone regardless of
miotic therapy, and this falls to 0% (0/25) in the absence of
miotics. Furthermore, any transient IOP rise with tropica-
mide tends to be modest, asymptomatic, and clinically
inconsequential [31].
Studies on eyes following iridectomy for acute
glaucoma
The management of acute glaucoma involves surgical
iridectomy or laser iridotomy with similar prophylaxis of
the fellow eye. Once a patent hole is achieved, the
obstruction to aqueous ow is eliminated and with it any
2000 Diabetes UK. Diabetic Medicine, 17, 693699
Review 697
risk of future angle closure. Mydriasis is then safe
whichever agent is used.
There are few studies on the effect of mydriasis on IOP in
these cases. In Harris and Galin's controlled study of 34
eyes with patent surgical iridectomies, cyclopentolate
induced a transient response (>6 mmHg IOP rise) in seven
cases (21%) [42]. Acute glaucoma did not occur, and
gonioscopy conrmed open angles throughout.
Phenylephrine did not cause an elevation of IOP. Very
similar results were given by Lowe [43,44]. Tropicamide
was not studied specically but was used uneventfully in
the 10 patients of the Baltimore survey who underwent
laser iridotomy [24].
Studies on untreated `high risk' fellow eyes
Epidemiological studies suggest that only a minority of
people with narrow anterior chamber angles, perhaps up to
10%, develop acute glaucoma [18]. However, untreated
fellow eyes in people who have had an episode of acute
glaucoma in one eye are at high risk. Studies indicate that
4570% of these eyes will develop acute glaucoma within
10 years if they are left untreated [4547].
Mapstone has studied the mechanics of angle closure in
untreated fellow eyes [2527,4752]. His studies show
that the precipitation of angle closure even in these highly
predisposed eyes is not an inevitable consequence of
mydriasis, but that it relates to the magnitude and duration
of the pupil blocking force. The latter is a function of the
iris sphincter and dilator vectors and the pupil size, with
miosis and wide mydriasis being positions of least threat,
and mid-dilation a position of greatest threat. In separate
studies with cyclopentolate, angle closure did not occur in
eight of 10 (80%) and in 12 of 21 untreated fellow eyes
(57%) [49,50]. In another study of 24 such eyes, all with
positive provocation tests, mydriasis with tropicamide
failed to produce a single case of angle closure [27].
Although Mapstone did report instances of incipient angle
closure with tropicamide in other series, he concluded that
tropicamide was much safer than the stronger agents in
these eyes. The pupil blocking force was much less and was
more easily overcome with treatment [5052].
It should be emphasized that fellow eyes are nowadays
treated routinely by iridotomy prophylaxis, so Mapstone's
work does not relate directly to the dilemma of mydriasis in
medical clinics. Nonetheless, his data provide reassurance:
even if these highly predisposed eyes were to be left
untreated, the risk of inducing acute glaucoma with
tropicamide alone would be very small.
Use of pilocarpine to reverse mydriasis
Pilocarpine eye drops are used commonly in medical clinics
to reverse mydriasis. This appears to be based on two
misconceptions. First, that the reduction of pupil size will
 698 Mydriasis and glaucoma: exploding the myth R. J. Pandit & R. Taylor
eliminate any risk of precipitating acute glaucoma, and
second, that it will hasten visual recovery. The evidence
however, indicates that the reverse is true in both instances.
Pilocarpine may induce angle closure in susceptible eyes
[27,5359]. This is because iris sphincter activity increases
the pupil blocking force, and ciliary body contraction
shallows the anterior chamber thereby compromising the
angle further. Pilocarpine following adrenergic mydriasis
with phenylephrine is particularly dangerous in susceptible
eyes. The iris dilator and sphincter vectors are maximal, the
position of mid-dilation is prolonged, and the anterior
chamber is shallowed. The risk of pupil block is therefore
high. Indeed, these phenomena form the basis of provoca-
tion tests using pilocarpine to identify eyes at risk of
developing angle closure [26,27,47,48].
Pilocarpine has little or no effect on the return of pupil
size, accommodation, or vision following anticholinergic
mydriasis [60,61]. In Nelson and Orton's controlled series,
vision actually deteriorated to 6/36 or worse in four of 23
eyes (17%) after pilocarpine was used for reversal [61].
Conclusions
Mydriasis with tropicamide is safe. There are no reports of
precipitation of acute glaucoma in the cited studies when
this agent is used alone in either a 0.5% or 1% solution.
The risk with long-acting or combined agents lies between
1 in 3380 and 1 in 20 000, and such events cannot be
predicted from the history. The common form of glaucoma
constitutes no additional risk of precipitating acute
glaucoma. Failure to dilate the pupil when fundoscopy is
indicated carries a greater danger of missing sight-
threatening disease. Tropicamide should be used in
medical clinics for all patients when thorough retinal
examination is indicated. As transient visual blurring will
be experienced by some but not all patients, this effect
should be mentioned in advance [6265]. Regarding the
remote possibility of acute glaucoma, prompt ophthalmo-
logical attention should be sought at any time if acute eye
pain or an excessive clouding of vision occur. The use of
pilocarpine to reverse mydriasis is potentially harmful and
should be avoided.
In a letter to the British Medical Journal in 1882,
Streatfeild wrote, `the present scare about the articial
production of glaucoma by use of mydriatics is much
exaggerated' [66]. The accumulated evidence over a
century later supports this view.
Key messages
Mydriasis with tropicamide is safe and should be
advised in all patients when thorough retinal examina-
tion is indicated.
A history of chronic (open angle) glaucoma does not
predispose to acute (angle closure) glaucoma following
mydriasis and should not contraindicate the use of
tropicamide.
The use of pilocarpine to reverse mydriasis is poten-
tially harmful and should be avoided.
Acknowledgements
The authors are grateful to Mr PG Grifths, Miss AJ
Dickinson, and Professor PD Home for their comments on
the manuscript.
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