Anterior capsulotomy is the main prostaglandin release inducer in FLACS

Take-home message: Research presented in this article found anterior capsulotomy to be the main trigger for an increase of prostaglandins in aqueous humor immediately after laser-assisted cataract surgery. Optimised energy settings in combination with NSAIDs might therefore help reduce laser-induced miosis.

By Faye Emery, OTE editor, Reviewed by Dr Burkhard Dick

The introduction of image-guided femtosecond lasers have resulted in several benefits, including a reduction in ultrasound energy and more precise capsulotomies.^1-4 However, for the first time, these devices also treat intraocular tissue, so their intraocular effects remain largely unknown. Several studies have reported the occurrence of laser-induced miosis shortly after laser treatment, with varying frequencies.^5-7

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Prostaglandins (especially prostaglandin E₂) play a role in inflammation-induced miosis and an increase in intraocular prostaglandin concentration immediately after laser treatment has previously been demonstrated.⁸ However, prior to the publication of the prospective study described in this article, which was carried out by Drs Tim Shultz, Stephanie C. Joachim, Mathias Stellbogen and Burkhard Dick,⁹ it was unclear which step of laser-assisted cataract surgery specifically causes release of prostaglandins. Understanding the specific mechanism involved in prostaglandin release is important as it can help us reduce its occurrence.

Assessing the relationship between prostaglandin concentration and FLACS

The purpose of the study was to investigate a possible correlation between intraocular prostaglandin concentrations and partial steps of laser-assisted cataract surgery. Specifically, the researchers were looking to see whether it was the fragmentation of the lens or the capsulotomy that induced inflammation after femtosecond laser-assisted surgery (FLACS).^10-13

Next: Anterior laser capsulotomy and prostaglandin stimulation

To test this, aqueous humor was collected from 67 patients after FLACS pretreatment (only capsulotomy, only fragmentation, or both) and again at the beginning of routine cataract surgery. Patients were randomly allocated to one of the four study groups and total prostaglandin levels were measured in each.

All surgeries were performed at the Institute for Vision Science, Ruhr University Eye Clinic, Bochum, Germany by Dr Dick. Preoperatively, all patients received the same topical medication. Medical mydriasis was induced using topical 0.5% tropicamide eye drops (Mydriati­cum; Stulln Pharma, Stulln, Germany) and 5.0% phen­ylepherine eye drops (Neo-Synephrine; Ursapharm, Saarbrücken, Germany) instilled three times within 1 hour prior to surgery. Oxybuprocaine eye drops (Con­juncain EDO 0.4%; Dr. Mann Pharma and Bausch & Lomb, Berlin, Germany) were applied three times for topical anesthesia 30 minutes prior to surgery.

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In the three laser-assisted cataract surgery groups (capsulotomy, fragmentation, and combination), dif­ferent steps of the procedure were performed using the Catalys Precision Laser System (Abbott Medical Optics, Santa Ana, California, USA). No corneal incisions were performed with the laser system. In the control group, a 1.2-mm paracentesis was created in the same manner as for the laser-assisted cataract surgery groups. Similar to the other groups, approximately 100 μL of aqueous humor was collected and immediately stored at -80°C. Routine manual cataract surgery with implantation of an IOL was then performed.

Anterior laser capsulotomy and prostaglandin stimulation

Surprisingly, findings indicated that anterior laser capsulotomy stimulates prostaglandin release. Investigators observed significantly higher prostaglandin lev­els after laser-assisted cataract surgery capsulotomy alone (362.4 ± 117.5 pg/mL; P = 0.01) and after capsulotomy in combina­tion with lens fragmentation (330.6 ± 110.6 pg/mL; P = 0.01) versus the control group (52.5 ± 8.1 pg/mL). La­ser-assisted cataract surgery fragmentation alone did not increase intraocular prostaglandin con­centration (186.8 ± 114.0 pg/mL; P = 0.14). This study is the first to identify anterior capsulotomy as the main trigger for an increase of prostaglandins in the aqueous humor immediately after laser-assisted cataract surgery.

Next: Possible explanation

It was previously suggested that the ciliary body releases prostaglandins in response to increased tem­perature, vibrations, or shockwaves.¹⁴ However, signifi­cantly more energy was used for lens fragmentation than capsulotomy (10 μJ versus 4 μJ, respectively) and treatment time for fragmen­tation was up to 20 times longer, which renders the tem­perature increase theory unlikely. A more likely scenario is that laser spots passing the aqueous humor in­duce vibrations or shockwaves, thereby presenting the main trigger for miosis.

Theses findings are important for surgeons to take note of, as optimising capsulot­omy laser settings has great potential to reduce the phenomenon of laser-induced miosis. A reduced incision depth in the anterior chamber during capsulotomy in combination with lower pulse energy appears to be of the utmost necessity. Furthermore, we can as­sume that the safety distance of the capsulotomy to the iris needs to be sufficient. A nonsteroidal anti-inflammatory drug (NSAID) pretreatment is likely to further decrease the incidence of laser-induced miosis.

Of interest, capsular block syn­drome occurred in none of the laser-assisted cataract surgery cases with fragmentation alone, which leads us to assume that our laser sys­tem settings results in either nonoccurrence or only rare occurrence of this complication. A possible explanation for this is the smaller numerical aperture of the Catalys Precision Laser System, which may result in less gas release.

References

• H.B. Dick and T. Schultz. J. Refract. Surg. 2014;30:198-201.

• I. Conrad-Hengerer et al., J. Refract. Surg. 2012;28:879-883.

• H.N. Dick and T. Schultz. J. Cataract Refract. Surg. 2013;39:1442-1444.

• N.J. Friedman et al., J. Cataract Refract. Surg. 2011;37:1189-1198.

• H.B. Dick, R.D. Gerste and T. Schultz. J Refract. Surg. 2013;29:662.

• R. Yeoh. J. Cataract Refract. Surg. 2014;40:852-853.

• S.J. Bali et al., Ophthalmology. 2012;119:891-899.

• T. Schultz et al., J. Refract. Surg. 2013;29:742-747.

• T. Schultz et al., J. Refract. Surg. 2015;31(2):78-81.

• K.D. Solomon et al., Arch. Ophthalmol. 1997;115:1119-1122.

• H.C. Keulen-de Vos et al., Br. J. Ophthalmol. 1983;67:94-96.

• H.V. Gimbel. Ophthalmology. 1989;96:585-588.

• F.A. Bucci Jr and L.D.Waterbury. Adv. Therapy. 2009;26:645-650.

• C. Maihofner et al., Invest. Ophthalmol. Vis. Sci. 2001;42:2616-2624.

Dr Burkhard Dick

E: dickburkhard@aol.com

Dr Dick is the Chairman & Director and Clinical Professor at the University Eye Hospital of Bochum, Germany.

Dr. Dick is a paid consultant for Abbott Medical Optics, Bausch & Lomb and Optical Express.