Transient-Drug-Induced-Myopia.pdf (original) (raw)

Non-steroidal drug-induced glaucoma

Eye, 2011

Numerous systemically used drugs are involved in drug-induced glaucoma. Most reported cases of non-steroidal drug-induced glaucoma are closed-angle glaucoma (CAG). Indeed, many routinely used drugs that have sympathomimetic or parasympatholytic properties can cause pupillary block CAG in individuals with narrow iridocorneal angle. The resulting acute glaucoma occurs much more commonly unilaterally and only rarely bilaterally. CAG secondary to sulfa drugs is a bilateral non-pupillary block type and is due to forward movement of iris-lens diaphragm, which occurs in individuals with narrow or open iridocorneal angle. A few agents, including antineoplastics, may induce open-angle glaucoma. In conclusion, the majority of cases with glaucoma secondary to non-steroidal medications are of the pupillary block closed-angle type and preventable if the at-risk patients are recognized and treated prophylactically.

The ocular adverse effects of oral drugs

Australian Prescriber

Some commonly prescribed drugs have ocular adverse effects. Many parts of the eye can be affected by oral drugs. Some ocular adverse effects may be reversed with medical or surgical intervention whereas other drugs may cause irreversible loss of vision. The risk of visual loss can be reduced by a number of approaches, including monitoring for ocular toxicity, reducing the drug dose, or stopping the drug and looking for an alternative. This can be supported by good communication between the prescribing clinician and ophthalmologist. Infrequent or delayed ocular adverse effects may not be identified in clinical trials of new drugs. Reporting adverse events is therefore important. may also cause corneal or scleral melting which requires urgent ophthalmology referral. Amiodarone, and other drugs such as hydroxychloroquine, can deposit on the basal epithelial layer of the cornea causing the formation of whirl-like corneal microdeposits called vortex keratopathy. 3 This is usually asymptomatic and does not require stopping the treatment. However, advanced corneal deposits can cause visual symptoms, hence patients should be referred for an ophthalmic review if the keratopathy affects their vision. Phenothiazines can cause the development of corneal epithelial changes that can eventually result in corneal oedema. The changes of corneal oedema can become permanent if the drug is not stopped promptly. 25 The long-term use of corticosteroids via any route of administration may increase intraocular pressure by interfering with the outflow from the trabecular meshwork. This is a significant risk factor for the development of glaucoma. 19 Iris and lens Corticosteroids can accelerate cataract progression. Classically, they cause posterior subcapsular cataracts which develop more rapidly than typical age-related nuclear sclerotic cataracts. 19 This may relate to corticosteroid-induced changes to gene transcription in the epithelial cells of the lens. 19 The long-term use of allopurinol has also been linked to cataract formation. 5 The use of alpha 1 adrenergic receptor antagonists, such as tamsulosin, may lead to the iris becoming mobile during cataract surgery, a phenomenon called intraoperative floppy iris syndrome. 2 The mechanism is probably related to the blockade of alpha 1 adrenergic receptors within the dilator muscle of the iris. Floppy iris syndrome may increase the likelihood of iris or posterior

A review of drug-induced acute angle closure glaucoma for non-ophthalmologists

Qatar Medical Journal, 2015

Acute angle closure glaucoma is an ophthalmic emergency and can lead to blindness if left untreated. Several types of drugs have the potential to precipitate acute angle closure glaucoma. These include adrenergic, cholinergic and anticholinergic, antidepressants, anticoagulants and sulfa-based agents. This article provides a basic overview of the risk factors and pathophysiologic mechanisms involved in angle closure glaucoma and focuses on drug-induced angle closure glaucoma for the non-ophthalmologist. A PubMed search limited to the English language was conducted to find relevant literature for the purpose of this article. Most attacks occur in subjects unaware that they are at risk due to innately narrow iridocorneal angles. Clinicians should always review medications in patients presenting with symptoms of acute angle closure glaucoma. The aim of this article is to bring this ophthalmic condition to the attention of clinicians, particularly those outside the field of ophthalmology who commonly prescribe these medications or see these patients prior to referring to ophthalmologists.

Indapamide-induced transient myopia with supraciliary effusion: case report

BMC Ophthalmology, 2013

Background: Ingestion of sulphonamide-derived drugs has been reported to possibly have ocular side-effects. Authors aimed to present a rare case of indapamide-induced transient myopia with ciliary body edema and supraciliary effusion. Case presentation: A 39 years old caucasian female patient presented at the Department of Neurology with headache and sudden bilateral loss of distant vision. Neurological assessment and cranial CT scans were unremarkable. For her hypertension, twice a day bisoprolol 2.5 mg and once a day indapamide 1.5 mg tablets were prescribed several days before. At her presenting, ophthalmic findings were as follows: visual acuity 0.08-7.25Dsph = 1.0 and 0.06-7.25Dsph = 1.0; IOP 25 mmHg and 24 mmHg, anterior chamber depth (ACD) 2.32 mm and 2.49 mm, lens thickness (L) 4.02 mm and 4.09 mm in the right and the left eye, respectively. By means of ultrasound biomicroscopy (UBM), thickened (720 / 700 micron) and detached ciliary body, its forward movement (ciliary body-cornea angle 108′ / 114′) and forward rotated ciliary processes were seen. Angle opening distance (AOD500) were 300 / 314 microns. By the following days, the myopia gradually diminished, and a week after her first symptoms, her uncorrected visual acuity was 1.0 in both eyes, IOP 13 mmHg and 17 mmHg, ACD 3.68 mm and 3.66 mm, L 3.78 mm and 3.81 mm in the right and the left eye, respectively. Ciliary body edema and detachment disappeared (ciliary body thickness 225 / 230 micron), both of the ciliary body-cornea angle 134′ / 140′ and the AOD500 (650 / 640 microns) increased. At this point, the patient admitted that she had stopped taking indapamide two days before. Conclusions: Our case report is the third one in the literature to present indapamide-induced transient myopia, and the first to employ UBM for describing the characteristics of this rare condition. According to the findings, authors suggest that both ciliary muscle contraction and ciliary body edema may play role in the pathomechanism. UBM seems to be a useful tool in the differential diagnosis of acute myopia. Further, authors wish to draw attention to one of the potential adverse effects of this drug which was not listed by its package insert.

Drug-induced Angle-Closure Glaucoma

Journal of Current Glaucoma Practice, 2012

Drug-induced angle-closure glaucoma is an important entity for the ophthalmologist as well as the general physician as it represents a preventable cause of potential blindness. This brief review highlights the fact that a high index of suspicion, in a susceptible individual followed by confirmation on appropriate imaging modality (UBM, ultrasound or anterior segment OCT) can alleviate the threat to sight and also help to institute appropriate therapy.

Drug-induced acute angle closure glaucoma

Current Opinion in Ophthalmology, 2007

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.

Drug-Induced Acute Angle-Closure Glaucoma: Raising your Index of Suspicion

Biomedical Journal of Scientific & Technical Research, 2021

Aim: To highlight polypharmacy as a risk factor for acute angle-closure glaucoma (AACG) in the emergency department (ED) with a brief literature review and propose an approach to early identification of AACG in the critically ill patients. Background: Acute angle-closure glaucoma (AACG) is an ophthalmological emergency that can lead to rapid, irreversible vision loss as a result of ischemia and atrophy of the optic nerve. Various drugs have been known to precipitate an acute angleclosure attack including adrenergics, anticholinergics, antihistamines, cholinergics, sulfonamides and serotonergic agents. Drug-induced AACG is usually observed in patients with predisposing risk factors. Anatomical risk factors include shallow chamber depth, small anterior segment and plateau iris configuration. Demographic risk factors include advanced age, family history, female gender and Asian ethnicity. Increasing rates of polypharmacy in the population, especially amongst the elderly, result in many patients with these predisposing risk factors also being on drugs that may precipitate AACG. More importantly, many drugs routinely prescribed acutely in the ED tend to overlap with the drugs reported to trigger AACG. Lastly, when an unresponsive patient presented to the ED, a diagnosis of AACG might be missed if the patient is unable to relay the classical symptoms. These three factors necessitate a high index of suspicion to ensure that a sight-threatening cause is not missed out in our patients.

Drug-Induced Uveitis

Survey of Ophthalmology, 1998

Uveitis has been reported in association with a variety of topical, intraocular, periocular, and systemic medications. To establish causality of adverse events by drugs, in 1981, Naranjo and associates proposed seven criteria, which are related to the frequency and documentation of the event; circumstances of occurrence, recovery, and recurrence; and coexistence of other factors or medications. Rarely does a drug meet all seven criteria. The authors review reports of drug-associated uveitis, applying the seven criteria and examining possible mechanisms. Only systemically administered biphosphonates and, perhaps, topical metipranolol meet all seven criteria. Systemic sulfonamides, rifabutin, and topical glucocorticoids fulfill at least five criteria.