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CORRESPONDENCE Intraoperative floppy-iris syndrome, a1-adrenergic antagonists, and chronic intake of mianserin: Is there an association? Marta Ugarte, DPhil, MRCOphth, Tony Leong, FRCOphth, Salwan Rassam, FRCS, FRCOphth, MD, Chee H. Kon, FRCS, FRCOphth, MD Intraoperative floppy-iris syndrome (IFIS) during phacoemulsification has been described in association with systemic a1-antagonists (eg, tamsulosin,1 alfuzosin,2 and doxazosin3). We report a case of IFIS in a 68-year-old white woman with chronic intake of the antidepressant mianserin. During preparation for phacoemulsification, the patient’s pupil dilated poorly with topical cyclopentolate 1% and phenylephrine 10%. In the medical history, it was noted she had taken mianserin, 20 mg, for 20 years. During the phacoemulsification procedure, the iris fluttered, billowed, and prolapsed to the phaco and side-port incisions and the pupil constricted gradually. The posterior capsule did not rupture, but iris damage resulted in pupil distortion, which required a pupilloplasty at a second stage to improve the symptoms of glare. Three weeks later, the uncorrected visual acuity was 6/9 and the glare had decreased. Mydriasis is mediated by activation of a1-receptors in the iris dilator muscle. Prolonged blockade of these receptors by systemic a1-antagonists may result in dilator tone loss, resistance to a1-agonists, and IFIS. The incidence of IFIS is unknown. An overall prevalence of 2% and 63% in patients on tamsulosin has been reported.1 For 20 years, our patient had been taking mianserin, an antidepressant with serotonin, histamine, and a1- and a2-adrenergic-receptor–blocking effects.4 Mianserin may, therefore, affect the iris dilator tone and predispose patients to IFIS. Because IFIS increases the risk for vitreous loss and iris trauma and typical mechanical stretching does not expand the pupil adequately in these eyes, recognition and anticipation of cases at risk for IFIS might reduce the complication rate. We raise the issue of IFIS associated with chronic intake of mianserin and encourage reports of similar cases and further studies to clarify this clinical entity. In the meantime, we consider it advisable to discontinue mianserin before cataract surgery.
REFERENCES 1. Chang DF, Campbell JR. Intraoperative floppy iris syndrome associated with tamsulosin. J Cataract Refract Surg 2005; 31:664–673 2. Settas G, Fitt AW. Intraoperative floppy iris syndrome in a patient taking alfuzosin for benign prostatic hypertrophy [letter]. In press, Eye 2006
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3. Helzner J. Managing floppy iris syndrome. Use of Flomax has been tied to this complication. Ophthalmol Management 2005; 9(4):22, 74. Available online at: http://www.ophmanagement.com/article.aspx?articleZ86311 4. Nalepa I, Vetulani J. The responsiveness of cerebral cortical adrenergic receptors after chronic administration of atypical antidepressant mianserin. J Psychiatry Neurosci 1994; 19:120–128
Labetalol causing intraoperative floppy-iris syndrome Fadi Calotti, MD, Daniel Steen, MD One month ago, while performing routine phacoemulsification surgery, we noticed that the patient’s pupil did not dilate well before surgery (only about 4.0 mm) despite standard preoperative pharmacologic dilation (topical cyclopentolate 1%, tropicamide 1%, phenylephrine 2.5%, and nonsteroidal antiinflammatory medication). We knew the patient’s history did not suggest a cause for the poor pupil dilation (miotic use, posterior synechias, trauma, diabetes mellitus) and also that she was not taking tamsulosin (Flomax) because we checked preoperatively, as part of our current routine. We were able to perform the capsulorhexis without stretching the pupil. After hydrodissection, we noticed a flaccid iris stroma that undulated and billowed in response to ordinary intraocular fluid currents and a propensity for the floppy iris stroma to prolapse toward the phaco and side-port incisions despite proper wound construction. The iris behavior was consistent with intraoperative floppy-iris syndrome (IFIS). The surgery was completed without complications. On review of the patient’s medication, we noted labetalol, an antihypertensive medication. It acts primarily as a b-blocker; the secondary effect is a1-blockade. We contacted the Clinical Pharmacology Department at Henry Ford Hospital to obtain a list of drugs that could potentially cause the same scenario through an a1-blocking effect. We were given the following list: prazosin (Minipress), terazosin (Hytrin), doxazosin (Cardura), tamsulosin (Flomax), alfuzosin (Uroxatral), phenoxybenzamine, phentolamine, labetalol (Trandate), carvedilol (Coreg), ergot derivatives (eg, ergotamine, dihydroergotamine), and some neuroleptic agents (eg, chlorpromazine and haloperidol). Although Chang and Campbell1 report that prazosin, terazosin, and doxazosin did not cause IFIS in their patients, more recent reports2 suggest the association of terazosin, doxazosin, and alfuzosin with IFIS. We now know that a-blockers vary in their selectivity for the a1- and a2-receptors and for different a1-receptor subtypes. Also, a1A-receptor is thought to be the predominant subtype in the iris dilator muscle (at least in rabbits3). We believe that labetalol probably has some a1A-subtype selectivity. We also think it would be a good practice to reevaluate the patient’s medication history if he/she shows signs of unexplained poor pupil dilation before surgery. We also suggest managing
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those taking any of the above medications as potential IFIS patients. REFERENCES 1. Chang DF, Campbell JR. Intraoperative floppy iris syndrome associated with tamsulosin. J Cataract Reftract Surg 2005; 31:664–673
2. Helzner J. Managing floppy iris syndrome. Use of Flomax has been tied to this complication. Ophthalmol Management 2005; 9(4):. 22, 74. Available online at: http://www.ophmanagement.com/article.aspx? articleZ86311 3. Nakamura S, Taniguchi T, Suzuki F, et al. Evaluation of a1–adrenoceptors in the rabbit iris: pharmacological characterization and expression of mRNA. Br J Pharmacol 1999; 127:1367–1374
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