The Effect of Suture Depth on Outflow Facility in Penetrating Keratoplasty

Zimmerman, Thom J.; Krupin, Theodore; Grodzki, Walter J.; Waltman, Stephen R.

doi:10.1001/archopht.1978.03910050273018

Cited by 66 publications

(29 citation statements)

References 5 publications

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“…Possible causes of increased IOP after DSEK include steroid use, retained viscoelastics, inflammation, peripheral anterior synechia (PAS), damage to the trabecular meshwork, and distortion of the angle with the collapse of the trabecular meshwork [11][12][13]. Early causes of postkeratoplasty IOP elevation include retained viscoelastics and inflammation.…”

Section: Discussionmentioning

confidence: 99%

Intraocular pressure elevation after Descemet’s stripping endothelial keratoplasty

et al. 2012

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Section: Discussionmentioning

confidence: 99%

Intraocular pressure elevation after Descemet’s stripping endothelial keratoplasty

et al. 2012

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“…Table 2 categorizes glaucoma risk by corneal diagnosis. Zimmerman demonstrated that full-thickness sutures approximating Descemet's membrane were not associated with changes in outflow facility, while midstromal bites decreased the outflow by 37% [129]. The size of the donor button in relation to the recipient bed was also proposed as a cause of increased IOP [128,130,131].…”

Section: Preoperative Considerationsmentioning

confidence: 99%

Graft failure: III. Glaucoma escalation after penetrating keratoplasty

Greenlee

Kwon

2008

Int Ophthalmol

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Glaucoma after penetrating keratoplasty is a frequently observed post-operative complication and is a risk factor for graft failure. Penetrating keratoplasty performed for aphakic and pseudophakic bullous keratopathy and inflammatory conditions are more likely to cause postoperative glaucoma compared with keratoconus and Fuchs' endothelial dystrophy. The intraocular pressure elevation may occur immediately after surgery or in the early to late postoperative period. Early postoperative causes of glaucoma include pre-existing glaucoma, retained viscoelastic, hyphema, inflammation, pupillary block, aqueous misdirection, or suprachoroidal hemorrhage. Late causes include pre-existing glaucoma, angle-closure glaucoma, ghost cell glaucoma, suprachoroidal hemorrhage, and steroid-induced glaucoma. Determining the cause of IOP elevation can help guide therapeutic intervention. Treatments for refractory glaucoma include topical anti-glaucoma medications such as beta-adrenergic blockers. Topical carbonic anhydrase inhibitors, miotic agents, adrenergic agonists, and prostaglandin analogs should be used with caution in the post-keratoplasty patient, because of the possibility of corneal decompensation, cystoid macular edema, or persistent inflammation. Various glaucoma surgical treatments have reported success in post-keratoplasty glaucoma. Trabeculectomy with mitomycin C can be successful in controlling IOP without the corneal toxicity noted with 5-fluorouracil. Glaucoma drainage devices have successfully controlled intraocular pressure in postkeratoplasty glaucoma; this is, however, associated with increased risk of graft failure. Placement of the tube through the pars plana may improve graft success compared with implantation within the anterior chamber. In addition, cyclophotocoagulation remains a useful procedure for eyes that have refractory glaucoma despite multiple surgical interventions.

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“…Zimmerman and co-workers using perfusion studies on cadaver eyes demonstrated that a corneal graft performed on a phakic eye did not appreciably alter the outflow facility when the host bed and donor were trephined to the same size, but in aphakic eyes the outflow facility was reduced by an average of 37 % , when midstromal suturing was employed, and not when through and through suturing was used. 5 The donor button size was also thought to be important and Zimmerman produced evidence to suggest that, in the aphakic patient, at least, the use of a donor button trephined with a trephine 0.5 mm larger than that used for the host bed reduced the incidence of PKPG. The effect was more obvious when a 7.5 mm trephine was used.6 Unfortunately, no account was taken of the real difference in size of excised buttons which may be produced by a change in intraocular pressure of the eye, or different pressures used when trephining or the differences which may be encountered due to varying corneal rigidity.…”

Section: Mechanismsmentioning

confidence: 99%