Comparison of triamcinolone acetonide, 11-deoxycortisol and other lipid formulae for the visualization of vitreous body in the anterior chamber after posterior capsule rupture in animal models.
OBJECTIVE
The efficacy and toxicity of triamcinolone acetonide and other lipid formulae--calcium palmitate, cholesterol and 11-deoxycortisol--in the visualization of the prolapsed vitreous body in the anterior chamber after posterior capsule rupture were investigated in animal models.


METHODS
In porcine eyes, a suspension of calcium palmitate, cholesterol, triamcinolone acetonide and 11-deoxycortisol was injected into the anterior chamber after intentionally creating posterior capsule rupture. Following gentle irrigation and aspiration, the vitreous body prolapsed in the anterior chamber was removed using an anterior vitrectomy cutter. In phakic rabbit eyes, the side-effects of the reagents were assessed for biomicroscopic appearance, intraocular pressure (IOP) and corneal histology.


RESULTS
The suspension of calcium palmitate, cholesterol, triamcinolone acetonide and 11-deoxycortisol was effective in the visualization of the vitreous body prolapsed in the anterior chamber after posterior capsule rupture. When cholesterol and calcium palmitate were injected into the anterior chamber, they remained there; this induced a significant increase in IOP and corneal oedema. In contrast, most of the triamcinolone acetonide and 11-deoxycortisol that was injected into the anterior chamber had disappeared a day after the injection without affecting IOP or corneal endothelial density. When injected into the intravitreous cavity, triamcinolone led to a significant increase in IOP 2 and 4 weeks after the injection. However, calcium palmitate, cholesterol and 11-deoxycortisol injected into the vitreous cavity had no effect on IOP at 4 weeks.


CONCLUSIONS
The suspension of triamcinolone acetonide and 11-deoxycortisol was effective in visualizing the vitreous body prolapsed in the anterior chamber after posterior capsule rupture. However, the amount of the reagent must be kept to a minimum to prevent the potential risk of ocular toxicities and postoperative late-onset ocular hypertension.
Kaji
Yuichi
Y
Department of Ophthalmology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan. sanken-tky@umin.ac.jp
Hiraoka
Takahiro
T
Okamoto
Fumiki
F
Asano
Hiroki
H
Oshika
Tetsuro
T
D000818:Animals; D000867:Anterior Chamber / Q000378:metabolism / Q000473:pathology*; D002784:Cholesterol / Q000009:adverse effects; D003315:Cornea / Q000473:pathology; D015715:Corneal Edema / Q000139:chemically induced; D003350:Cortodoxone / Q000008:administration & dosage / Q000493:pharmacokinetics; D066298:In Vitro Techniques; D007267:Injections; D007429:Intraocular Pressure / Q000187:drug effects; D007903:Lens Capsule, Crystalline / Q000293:injuries*; D008055:Lipids / Q000008:administration & dosage / Q000493:pharmacokinetics; D008297:Male; D008853:Microscopy / Q000379:methods; D019308:Palmitic Acid / Q000009:adverse effects; D011391:Prolapse; D011817:Rabbits; D012421:Rupture / Q000473:pathology / Q000503:physiopathology; D013552:Swine; D014222:Triamcinolone Acetonide / Q000008:administration & dosage / Q000009:adverse effects / Q000493:pharmacokinetics; D014822:Vitreous Body / Q000473:pathology*
D008055:Lipids; D019308:Palmitic Acid; D002784:Cholesterol; D014222:Triamcinolone Acetonide; D003350:Cortodoxone