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Drug-induced acute angle closure glaucomaYves Lachkar and Walid Bouassida Acute angle closure glaucoma is a potentially blinding Acute angle closure glaucoma (AACG) occurs in pre- side effect of a number of local and systemic drugs, disposed individuals (hypermetropia, narrow angle, thick including adrenergic, both anticholinergic and cholinergic, lens) when the pupil is mid dilated. At least one-third of antidepressant and antianxiety, sulfa-based, and AACG cases are related to an over-the-counter or pre- anticoagulant agents. The purpose of this article is to bring scription drug. Drugs with a1 adrenergic or anticholiner- this condition to the attention of clinicians using these gic effects can precipitate attacks of AACG mainly by compounds as well as ophthalmologists called to see the mydriasis. Some drugs with no pupillary effect induce AACG by ciliochoroidal effusion (sulpha-based drugs and anticoagulants). The new term ‘acute angle closure crisis’ Acute angle closure glaucoma due to pupillary block, replaces the former ‘acute angle closure glaucoma’ when treatable by peripheral iridotomy, can be caused by no glaucomatous optic nerve damage is observed before adrenergic agents, either locally (phenylephrine drops, the attack We will use both terms in this review.
nasal ephedrine, or nebulized salbutamol) or systemically(epinephrine for anaphylactic shock), drugs with Both local (ocular drops, nasal and nebulized agents) anticholinergic effects including tropicamide and atropine and systemic drugs (e.g. atropine, adrenaline, ephedrine, drops, tri and tetracyclic antidepressants, and cholinergic some psychoactive and antiepileptic drugs) can induce agents like pilocarpine. A novel anticholinergic form is the AACG. Using the PubMed database we reviewed the use of periocular botulinum toxin diffusing back to the ciliary most recent articles (case reports and reviews) published ganglion inhibiting the pupillary sphincter. Sulfa-based drugs (acetazolamide, hydrochlorothiazide, cotrimoxazole,and topiramate) can cause acute angle closure glaucoma Drugs that can induce AACG should be recognized not by ciliary body edema with anterior rotation of the iris-lens only because of the risk of AACG but also because certain diaphragm. Iridotomy is not effective.
drugs can induce intermittent angle closure or exacerbate Most attacks of acute angle closure glaucoma involvingpupillary 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 precipitate an attack of acute AACG in predisposed individuals that have shallow anterior chambers. Phenyl-ephrine drops are commonly used to induce pupillary dilation for ocular fundus examination and may induce acute angle closure glaucoma, adrenergic drugs, central AACG in about 0.03% of nonselected patients .
France) is an a2-adrenergic agent that has a minor a1 Curr Opin Ophthalmol 18:129–133. ß 2007 Lippincott Williams & Wilkins.
effect, causing mild mydriasis We observed twocases of AACG caused or precipitated by apraclonidine Department of Ophthalmology, Glaucoma Institute, Saint Joseph Hospital, Paris,France drops in predisposed patients (personal report, not pub-lished). Dipivephrine (Propine: Allergan France Sas, Correspondence to Doctor Yves Lachkar, Department of Ophthalmology,Glaucoma Institute, Saint Joseph Hospital, 185, rue Raymond Losserand, 75674 Mougins, France) also has a mild mydriatic effect.
Paris Cedex 14, FranceTel: +33 1441 23420; e-mail: Cases of AACG have been reported after systemic admin- Current Opinion in Ophthalmology 2007, 18:129–133 istration of ephedrine for flu, surgical anaesthesia or epinephrine (adrenaline) to treat anaphylactic shock and ventricular fibrillation. Intake of nasal ephedrineand naphazoline in the acute management of epistaxis ß 2007 Lippincott Williams & Wilkins can induce AACG, which may be bilateral AACG is believed to result more from the reflux through theipsilateral nasolacrimal duct than from the absorptionthrough the nasal mucosa, even though plasma levels Copyright Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
can be similar to those achieved with intravenous admin- glaucoma attacks. Ates et al. recommend practising an oblique penlight illumination test by anaesthesiolo-gists to estimate anterior chamber depth and determine Nebulized b2-adrenergic agents (salbutamol, albuterol, the population at risk. Patients at risk for AACG in the terbutaline) are used for bronchodilation in patients with postoperative period can be administered topical pilocar- asthma or chronic obstructive pulmonary disease. They pine therapy to prevent any attack. Since symptoms of can increase the intraocular pressure and induce transient AACG may be overlooked or misinterpreted in a sedated angle closure. Stimulating ciliary body b2-adrenergic or comatose patient, any patient who has a red eye receptors promotes aqueous humour secretion. Angle and a subjective vision loss postoperatively should be closure is exacerbated by pupil dilation caused by the parasympathetic inhibitory effect of ipratropium, especi-ally when an anticholinergic drug is frequently connected Corridan et al. reported a case of AACG which These drugs can be absorbed through the cornea occurred shortly after a series of injections of botulinum and the conjunctiva after escaping from a face mask.
toxin around the eyelids for blepharospasm. Botulinum Properly fitted and positioned masks and hand-held toxin injected periocularly diffuses towards the ciliary nebulizers can minimize ocular deposition of nebulized ganglion and there impedes the cholinergic innervation of the pupil. This complication, though rare, should betaken into consideration in predisposed patients who Some other drugs that have indirect sympathomimetic activity can induce AACG: amphetamines, some anti-depressant agents (imipramine, monoamine oxidase inhibitors), cocaine, especially when used intranasally Pilocarpine is used in some forms of glaucoma to constrict the pupil and increase aqueous outflow through the majoroutflow pathways. It can, however, induce AACG due to anterior movement of the iris-lens diaphragm, thus result- Tropicamide is a short-acting anticholinergic commonly ing in complete angle closure Eyes with zonular used to induce pupil dilation for fundus examination.
weakness or exfoliation syndrome seem to be particularly Atropine, homatropine and cyclopentolate used to relax prone to developing miotic-induced angle closure the ciliary muscle and dilate the pupil have long-acting Ritch et al. reported chronic angle closure developing anticholinergic action, and more frequently induce AACG after several years of miotic therapy in eyes that initially Ipratropium bromide (Atrovent: Boehringer Ingelheim Acetylcholine and carbachol are topical medications used France, Paris, France) is an antimuscarinic drug usually to constrict the pupil during intraocular surgery, especi- prescribed in combination with salbutamol in acute ally cataract extraction. They can induce pupillary block exacerbation of chronic obstructive pulmonary disease.
Many cases of AACG associated with nebulized ipratro-pium have been reported Fifty percent of patients with preexisting narrow angles who received a Tri and tetracyclic antidepressants are known to have nebulized salbutamol and ipratropium combination important anticholinergic side effects. They have fre- manifest transient AACG As supposed for aeroso- quently been associated with AACG in predisposed lized b2-adrenergic agents, ipratropium escapes from the face mask, diffuses through the cornea producing pupildilation and, in eyes with susceptible angles, angle Selective serotonin reuptake inhibitors (SSRIs) have a lower incidence of cholinergic side effects than tricyclicantidepressants. Nevertheless, many reports of AACG Atropine is often used to treat bradycardia, especially associated with paroxetine , venlafaxine related to general anaesthesia. Postoperative AACG was reported in patients after general anaesthesia for abdomi- were reported. The weak anticholinergic and adre- nal, orthopaedic, facial and endoscopic surgery nergic activity and the mydriatic effect of increased Several factors are likely to induce postoperative AACG levels of serotonin are possible mechanisms of AACG.
in predisposed individuals: anticholinergic drugs (atro- De Guzman et al. and Zelefsky et al. have pine, scopolamine, and muscle relaxants), adrenergic identified by ultrasonography supraciliary effusion that drugs (ephedrine, epinephrine). Moreover, the peropera- precipitates the AACG. Ophthalmological consultations tive period carries the risk of psychological stress and should be considered before starting treatment with SSRIs darkness-induced mydriasis that may increase the risk of Copyright Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Drug-induced acute angle closure glaucoma Lachkar and Bouassida heparin and low molecular weight heparin (enoxaparin, Some sulfa-based drugs have been associated with rare warfarin) have been reported to cause AACG.
AACG: acetazolamide hydrochlorothiazide andcotrimoxazole To manage increased intraocular pressure, anticoagula-tive treatment should be discontinued and the symptoms Topiramate is a sulfamate-substituted monosaccharide managed as for AACG. Peripheral iridotomy is not effec- antiepileptic agent. Since it was approved in 1995, several tive in the management. Surgery may be needed to drain case reports have been published addressing its ocular side effects, including AACG, transient myopia and uveal effu-sion The majority of adverse cases have occurred in females (89%), in paediatric patients as Histamine H1 receptor antagonists (brompheniramine, well as adults. Eighty-five percent of cases occurred in chlorpheniramine, dexbrompheniramine, dexchlorphen- the first 3 weeks of treatment with topiramate, in five iramine, dimethindene, pheniramine, triprolidine) are cases within hours after doubling the dose and in only used to treat manifestations of allergic disease. Histamine one case it occurred 49 days from the onset of therapy H2 receptor antagonists (cimetidine, ranitidine) are usedto treat gastroesophageal reflux and duodenal ulcers. Both Patients were typically taking topiramate doses within of them have a weak anticholinergic effect, which can the normal therapeutic range. In only a few cases was the induce mydriasis and AACG in predisposed patients presentation unilateral. No risk factors are known for thissyndrome Other drugsOne case of recurrent bilateral AACG after combined The underlying mechanism has been better character- consumption of ‘ecstasy’, a synthetic amphetamine deri- ized with ultrasound technology. Ciliary body oedema vate, and marijuana in a 29-year-old women was reported causes relaxation of the zonules, which allows lens Ecstasy increases the release of monoamine neuro- thickening. Anterolateral rotation of the ciliary body transmitters (serotonin, noradrenaline and dopamine) and about its attachment to the scleral spur leads to anterior inhibits the uptake of serotonin from the synaptic gap.
displacement of the lens and iris and concomitant It induces mydriasis and AACG in predisposed persons.
shallowing of the anterior chamber. Choroidal detach-ment and supraciliary effusion are frequently present.
Yalvac reported two cases of AACG in association with Secondary angle closure glaucoma occurs without pupil- topical administration of latanoprost . He speculates lary block, therefore peripheral iridotomies are ineffec- that latanoprost induces a swelling of the ciliary muscle, pushing the iris-lens diaphragm anteriorly and initiatingthe AACG in predisposed patients.
Fluid movement in choroidal effusion could be related todrug-induced changes in membrane potential associatedwith topiramate. The finding of effusion in only a few patients taking topiramate, however, suggests that it is an A variety of drugs can cause AACG in susceptible indi- The management of topiramate-related AACG requires Table 1 Classification of drugs inducing acute angle closure stopping the drug in concert with the prescribing physi- cian, because decreasing the dose may exacerbate pre- existing 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 If unrecognized as a drug- related event, serious outcomes could occur (seven cases of permanent vision loss have been reported).
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 Both Copyright Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
play, including pupillary block for which a peripheral 12 Hall SK. Acute angle-closure glaucoma as a complication of combined beta- agonist and ipratropium bromide therapy in the emergency department. Ann iridectomy can be curative, ciliary or suprachoroidal effusion, or even vitreous haemorrhage with forward 13 De Saint Jean M, Boursier T, Borderie V. Acute closure-angle glaucoma after movement of the iris-lens diaphragm and shallowing of treatment with ipratropium bromide and salbutamol aerosols. J Fr Ophthalmol2000; 23:603–605.
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Drug-induced acute angle closure glaucoma Lachkar and Bouassida 39 Fraunfelder FW, Fraunfelder FT. Adverse ocular drug reactions recently 46 Banta JT, Hoffman K, Budenz DL, et al. Presumed topiramate-induced identified by the National Registry of Drug-Induced Ocular Side Effects.
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52 Berdy GJ, Berdy SS, Odin LS, et al. Angle closure glaucoma precipitated by 45 Ikeda N, Ikeda T, Nagata M, et al. Ciliochoroidal effusion syndrome induced by aerosolized atropine. Arch Intern Med 1992; 151:1658 –1660.
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