Download Drug-induced acute angle closure glaucoma

Drug-induced acute angle closure glaucoma
Yves Lachkar and Walid Bouassida
Purpose of review
Acute angle closure glaucoma is a potentially blinding
side effect of a number of local and systemic drugs,
including adrenergic, both anticholinergic and cholinergic,
antidepressant and antianxiety, sulfa-based, and
anticoagulant agents. The purpose of this article is to bring
this condition to the attention of clinicians using these
compounds as well as ophthalmologists called to see the
patient.
Recent findings
Acute angle closure glaucoma due to pupillary block,
treatable by peripheral iridotomy, can be caused by
adrenergic agents, either locally (phenylephrine drops,
nasal ephedrine, or nebulized salbutamol) or systemically
(epinephrine for anaphylactic shock), drugs with
anticholinergic effects including tropicamide and atropine
drops, tri and tetracyclic antidepressants, and cholinergic
agents like pilocarpine. A novel anticholinergic form is the
use of periocular botulinum toxin diffusing back to the ciliary
ganglion inhibiting the pupillary sphincter. Sulfa-based
drugs (acetazolamide, hydrochlorothiazide, cotrimoxazole,
and topiramate) can cause acute angle closure glaucoma
by ciliary body edema with anterior rotation of the iris-lens
diaphragm. Iridotomy is not effective.
Summary
Most attacks of acute angle closure glaucoma involving
pupillary block occur in individuals that are unaware that
they have narrow iridocorneal angles. Practitioners using
any of the above drugs should be aware of their potential to
cause acute angle closure.
Keywords
acute angle closure glaucoma, adrenergic drugs, central
nervous system drugs, drug
Curr Opin Ophthalmol 18:129–133. ß 2007 Lippincott Williams & Wilkins.
Department of Ophthalmology, Glaucoma Institute, Saint Joseph Hospital, Paris,
France
Correspondence to Doctor Yves Lachkar, Department of Ophthalmology,
Glaucoma Institute, Saint Joseph Hospital, 185, rue Raymond Losserand, 75674
Paris Cedex 14, France
Tel: +33 1441 23420; e-mail: [email protected]
Current Opinion in Ophthalmology 2007, 18:129–133
Abbreviation
AACG
acute angle closure glaucoma
ß 2007 Lippincott Williams & Wilkins
1040-8738
Introduction
Acute angle closure glaucoma (AACG) occurs in predisposed individuals (hypermetropia, narrow angle, thick
lens) when the pupil is mid dilated. At least one-third of
AACG cases are related to an over-the-counter or prescription drug. Drugs with a1 adrenergic or anticholinergic effects can precipitate attacks of AACG mainly by
mydriasis. Some drugs with no pupillary effect induce
AACG by ciliochoroidal effusion (sulpha-based drugs and
anticoagulants). The new term ‘acute angle closure crisis’
replaces the former ‘acute angle closure glaucoma’ when
no glaucomatous optic nerve damage is observed before
the attack [1]. We will use both terms in this review.
Both local (ocular drops, nasal and nebulized agents)
and systemic drugs (e.g. atropine, adrenaline, ephedrine,
some psychoactive and antiepileptic drugs) can induce
AACG. Using the PubMed database we reviewed the
most recent articles (case reports and reviews) published
in English, French and German.
Drugs that can induce AACG should be recognized not
only because of the risk of AACG but also because certain
drugs can induce intermittent angle closure or exacerbate
chronic angle closure glaucoma.
Adrenergic agents
Alpha-adrenergic agents cause mydriasis that can
precipitate an attack of acute AACG in predisposed
individuals that have shallow anterior chambers. Phenylephrine drops are commonly used to induce pupillary
dilation for ocular fundus examination and may induce
AACG in about 0.03% of nonselected patients [2,3].
Apraclonidine (Iopidine: Alcon, Rueil-Malmaison,
France) is an a2-adrenergic agent that has a minor a1
effect, causing mild mydriasis [4,5]. We observed two
cases of AACG caused or precipitated by apraclonidine
drops in predisposed patients (personal report, not published). Dipivephrine (Propine: Allergan France Sas,
Mougins, France) also has a mild mydriatic effect.
Cases of AACG have been reported after systemic administration of ephedrine for flu, surgical anaesthesia or
epinephrine (adrenaline) to treat anaphylactic shock
and ventricular fibrillation. Intake of nasal ephedrine
and naphazoline in the acute management of epistaxis
can induce AACG, which may be bilateral [6,7]. AACG is
believed to result more from the reflux through the
ipsilateral nasolacrimal duct than from the absorption
through the nasal mucosa, even though plasma levels
129
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130 Glaucoma
can be similar to those achieved with intravenous administration [8].
Nebulized b2-adrenergic agents (salbutamol, albuterol,
terbutaline) are used for bronchodilation in patients with
asthma or chronic obstructive pulmonary disease. They
can increase the intraocular pressure and induce transient
angle closure. Stimulating ciliary body b2-adrenergic
receptors promotes aqueous humour secretion. Angle
closure is exacerbated by pupil dilation caused by the
parasympathetic inhibitory effect of ipratropium, especially when an anticholinergic drug is frequently connected
[9–13]. These drugs can be absorbed through the cornea
and the conjunctiva after escaping from a face mask.
Properly fitted and positioned masks and hand-held
nebulizers can minimize ocular deposition of nebulized
medication.
Some other drugs that have indirect sympathomimetic
activity can induce AACG: amphetamines, some antidepressant agents (imipramine, monoamine oxidase
inhibitors), cocaine, especially when used intranasally
[8,14,15]
Anticholinergic agents
Tropicamide is a short-acting anticholinergic commonly
used to induce pupil dilation for fundus examination.
Atropine, homatropine and cyclopentolate used to relax
the ciliary muscle and dilate the pupil have long-acting
anticholinergic action, and more frequently induce AACG
[16,17].
Ipratropium bromide (Atrovent: Boehringer Ingelheim
France, Paris, France) is an antimuscarinic drug usually
prescribed in combination with salbutamol in acute
exacerbation of chronic obstructive pulmonary disease.
Many cases of AACG associated with nebulized ipratropium have been reported [10–13]. Fifty percent of
patients with preexisting narrow angles who received a
nebulized salbutamol and ipratropium combination
manifest transient AACG [11]. As supposed for aerosolized b2-adrenergic agents, ipratropium escapes from the
face mask, diffuses through the cornea producing pupil
dilation and, in eyes with susceptible angles, angle
closure [10].
Atropine is often used to treat bradycardia, especially
related to general anaesthesia. Postoperative AACG was
reported in patients after general anaesthesia for abdominal, orthopaedic, facial and endoscopic surgery [18].
Several factors are likely to induce postoperative AACG
in predisposed individuals: anticholinergic drugs (atropine, scopolamine, and muscle relaxants), adrenergic
drugs (ephedrine, epinephrine). Moreover, the peroperative period carries the risk of psychological stress and
darkness-induced mydriasis that may increase the risk of
glaucoma attacks. Ates et al. [19] recommend practising
an oblique penlight illumination test by anaesthesiologists to estimate anterior chamber depth and determine
the population at risk. Patients at risk for AACG in the
postoperative period can be administered topical pilocarpine therapy to prevent any attack. Since symptoms of
AACG may be overlooked or misinterpreted in a sedated
or comatose patient, any patient who has a red eye
and a subjective vision loss postoperatively should be
examined urgently.
Corridan et al. [20] reported a case of AACG which
occurred shortly after a series of injections of botulinum
toxin around the eyelids for blepharospasm. Botulinum
toxin injected periocularly diffuses towards the ciliary
ganglion and there impedes the cholinergic innervation
of the pupil. This complication, though rare, should be
taken into consideration in predisposed patients who
undergo this procedure.
Cholinergic agents
Pilocarpine is used in some forms of glaucoma to constrict
the pupil and increase aqueous outflow through the major
outflow pathways. It can, however, induce AACG due to
anterior movement of the iris-lens diaphragm, thus resulting in complete angle closure [16]. Eyes with zonular
weakness or exfoliation syndrome seem to be particularly
prone to developing miotic-induced angle closure [21].
Ritch et al. [22] reported chronic angle closure developing
after several years of miotic therapy in eyes that initially
had wide open angles.
Acetylcholine and carbachol are topical medications used
to constrict the pupil during intraocular surgery, especially cataract extraction. They can induce pupillary block
in susceptible patients [16].
Antidepressants, antianxiety agents
Tri and tetracyclic antidepressants are known to have
important anticholinergic side effects. They have frequently been associated with AACG in predisposed
individuals [21,23,24].
Selective serotonin reuptake inhibitors (SSRIs) have a
lower incidence of cholinergic side effects than tricyclic
antidepressants. Nevertheless, many reports of AACG
associated with paroxetine [25–29], venlafaxine [30,31,
32], fluvoxamine [33], citalopram [34] and escitalopram
[35] were reported. The weak anticholinergic and adrenergic activity and the mydriatic effect of increased
levels of serotonin are possible mechanisms of AACG.
De Guzman et al. [30] and Zelefsky et al. [35] have
identified by ultrasonography supraciliary effusion that
precipitates the AACG. Ophthalmological consultations
should be considered before starting treatment with SSRIs
in predisposed patients [36].
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Drug-induced acute angle closure glaucoma Lachkar and Bouassida 131
Sulfa-based drugs
Some sulfa-based drugs have been associated with rare
AACG: acetazolamide [16], hydrochlorothiazide [37], and
cotrimoxazole [16].
Topiramate is a sulfamate-substituted monosaccharide
antiepileptic agent. Since it was approved in 1995, several
case reports have been published addressing its ocular side
effects, including AACG, transient myopia and uveal effusion [38–42,43,44,45]. The majority of adverse cases
have occurred in females (89%), in paediatric patients as
well as adults. Eighty-five percent of cases occurred in
the first 3 weeks of treatment with topiramate, in five
cases within hours after doubling the dose and in only
one case it occurred 49 days from the onset of therapy [39].
Patients were typically taking topiramate doses within
the normal therapeutic range. In only a few cases was the
presentation unilateral. No risk factors are known for this
syndrome [41].
The underlying mechanism has been better characterized with ultrasound technology. Ciliary body oedema
causes relaxation of the zonules, which allows lens
thickening. Anterolateral rotation of the ciliary body
about its attachment to the scleral spur leads to anterior
displacement of the lens and iris and concomitant
shallowing of the anterior chamber. Choroidal detachment and supraciliary effusion are frequently present.
Secondary angle closure glaucoma occurs without pupillary block, therefore peripheral iridotomies are ineffective [43,45,46].
Fluid movement in choroidal effusion could be related to
drug-induced changes in membrane potential associated
with topiramate. The finding of effusion in only a few
patients taking topiramate, however, suggests that it is an
idiosyncratic reaction [43].
The management of topiramate-related AACG requires
stopping the drug in concert with the prescribing physician, because decreasing the dose may exacerbate preexisting systemic conditions. In all reported cases, none
has subsided without discontinuation of the drug. If the
drug is stopped and medical management is instituted,
however, intraocular pressure may return to normal in a
period of hours to days [37,38]. If unrecognized as a drugrelated event, serious outcomes could occur (seven cases
of permanent vision loss have been reported).
Anticoagulants
Acute secondary angle closure glaucoma after massive
vitreous, choroidal or subretinal haemorrhage is a rare
complication of anticoagulant therapy. Risk factors are
overtreatment with anticoagulants, exudative age-related
macular degeneration and nanophthalmos [47–49]. Both
heparin and low molecular weight heparin (enoxaparin,
warfarin) have been reported to cause AACG.
To manage increased intraocular pressure, anticoagulative treatment should be discontinued and the symptoms
managed as for AACG. Peripheral iridotomy is not effective in the management. Surgery may be needed to drain
choroidal effusion or haemorrhage [46].
Histamine H1 and H2 receptor antagonists
Histamine H1 receptor antagonists (brompheniramine,
chlorpheniramine, dexbrompheniramine, dexchlorpheniramine, dimethindene, pheniramine, triprolidine) are
used to treat manifestations of allergic disease. Histamine
H2 receptor antagonists (cimetidine, ranitidine) are used
to treat gastroesophageal reflux and duodenal ulcers. Both
of them have a weak anticholinergic effect, which can
induce mydriasis and AACG in predisposed patients [16].
Other drugs
One case of recurrent bilateral AACG after combined
consumption of ‘ecstasy’, a synthetic amphetamine derivate, and marijuana in a 29-year-old women was reported
[50]. Ecstasy increases the release of monoamine neurotransmitters (serotonin, noradrenaline and dopamine) and
inhibits the uptake of serotonin from the synaptic gap.
It induces mydriasis and AACG in predisposed persons.
Yalvac reported two cases of AACG in association with
topical administration of latanoprost [51]. He speculates
that latanoprost induces a swelling of the ciliary muscle,
pushing the iris-lens diaphragm anteriorly and initiating
the AACG in predisposed patients.
Conclusion
A variety of drugs can cause AACG in susceptible individuals (Table 1) [52]. Different mechanisms may be at
Table 1 Classification of drugs inducing acute angle closure
glaucoma by administration route
Eye drops
Mydriatics
Local drugs
In the anterior
chamber
Intranasal
Periocular
Aerosolized drugs
Systemic
drugs
Vegetative nerve
system drugs
Anticoagulants
Central nerve
system drugs
Diuretics
Other drugs
Phenylephrine, tropicamide,
atropine, homatropine,
cyclopentolate
Acetylcholine, carbachol
Ephedrine, naphazoline, cocaine
Botulinum toxin
Salbutamol, albuterol, terbutaline,
ipratropium bromide, atropine
[52]
Ephedrine, epinephrine (adrenaline)
Heparin, warfarin, enoxaparin
Topiramate, amphetamines, some
antidepressant agents
Acetazolamide, hydrochlorothiazide
Cotrimoxazol, histamine H1 and
H2 receptor antagonists
Source: Tripathi et al. [16].
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132 Glaucoma
play, including pupillary block for which a peripheral
iridectomy can be curative, ciliary or suprachoroidal
effusion, or even vitreous haemorrhage with forward
movement of the iris-lens diaphragm and shallowing of
the anterior chamber. Iridectomy for these latter causes
is ineffective.
The problem is to know which eye is at risk. Most attacks
involving pupillary block occur in individuals that are
unaware that they have narrow iridocorneal angles. Physicians using these drugs cannot practically send each and
every patient to an ophthalmologist for gonioscopy and it
is not helpful to ask the patient if they have glaucoma
since they would be asymptomatic. With open angle
glaucoma, there is virtually no risk of AACG. With angle
closure glaucoma already treated by iridotomy, filtering
surgery, or cataract extraction, there is also no real risk.
There is no ideal solution to the problem except to warn
medical practitioners to be wary of patients wearing thick
hyperopic glasses that magnify objects. One could also
recommend use of the lateral penlight method to estimate anterior chamber depth.
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