Review and Update of Intraoperative Floppy Iris Syndrome

Ahmed Sallam; Hany El-Defrawy; Adam Ross; Samer J Bashir; Hamish MA Towler

Disclosures

Expert Rev Ophthalmol. 2011;6(4):469-476. 

In This Article

Underlying Mechanisms of IFIS

Current thinking for the occurrence of IFIS with tamsulosin is mainly based on pharmacological blockade of the α1 receptors present in the iris.[28–30] Evidence shows that, similar to prostate, postsynaptic α-1 adrenergic receptors predominate in iris dilator smooth muscle and that stimulation of this receptor subtype mediates muscle contraction and pupil dilatation.[29,30] By contrast, α-1a blockade results in relaxation of the dilator muscle with poor pupillary dilatation. Chang and Campbell proposed that iris billowing and prolapse in IFIS are probably due to loss of the dilator muscle tone, which normally confers iris rigidity.[9]

No study has established a minimum duration of intake of tamsulosin leading to IFIS. However, there are several reports suggesting that IFIS can occur within weeks of commencing tamsulosin[17,18] and one case report showed that IFIS can develop as early as 2 days after treatment.[31] Tamsulosin has a long half-life, with detectable levels in the aqueous humor of patients who stopped the medication up to 28 days previously.[19] Nevertheless, discontinuation of tamsulosin therapy preoperatively for periods longer than 28 days (and sometimes for several years) does not necessarily eliminate the occurrence of IFIS.[9] A plausible explanation that constant blockade of the iris dilator muscle by tamsulosin may result in permanent disuse atrophy of the muscle.[9] Evidence for this assumption can be drawn from a histological study of cadaver eyes that showed decreased iris dilator muscle thickness in patients receiving tamsulosin compared with a control group,[29] as well as a further study that demonstrated thinning of dilator muscle region in tamsulosin patients when examined by optical coherence tomography.[32] A recent immunohistochemical study of iris tissue from a patient with tamsulosin-related IFIS undergoing glaucoma surgery provided some evidence to suggest that IFIS may also develop owing to vascular dysfunction.[30] In addition to the dilator muscle, localization of α-1a receptors in iris arteriolar muscularis was demonstrated in this report. However, histological thickness and structure of the iris dilator muscle were normal. The authors suggested that tamsulosin-induced dysfunction at the level of iris vessels can lead to loss of the ability of the iris vessels to coil resulting in poor pupillary dilatation and iris flaccidity.[30]

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