Intraocular Pressure Changes after Triamcinolone Acetonide Intravitreal Injection
←
→
Page content transcription
If your browser does not render page correctly, please read the page content below
Med. J. Cairo Univ., Vol. 79, No. 2, December: 147-151, 2011
www.medicaljournalofcairouniversity.com
Intraocular Pressure Changes after Triamcinolone Acetonide
Intravitreal Injection
HOSSAM EL-DIN KHALIL, M.D.*; WALEEDMAHRAN, M.D.*; HAZEM HAROUN, M.D.*;
HOSSAM BEKEIR, M.D.* and AHMED EL-SHAFIE, M.Sc.**
The Departments of Ophthalmology, Beni-Swif University* and Ophthalmplogist, Rod El-Farag Hospital**
Abstract (range 13-24mmHg) postoperatively. 5 (12.5%) of patients
in group B showed significant elevation of IOP (>25mmHg)
Aim: To investigate the intraocular pressure (IOP) respon- after topical administration of prednisolone acetate and were
seafter intravitreal triamcinolone acetonide (IVTA) injections excluded from injection. 4 of them were managed by topical
astreatment of intraocular neovascular or oedematous diseases B-blockers, and 1 eye required trabeculoplasty. Preoperative
and the ability to predict secondary steroid-induced glaucoma. predictive factor for the rise in IOP was younger age
(p=0.0002). It was statistically independent of refractive error,
Methods: The prospective consecutive comparative inter- presence of diabetes mellitus, and indication for the injection.
ventional case series study included 80 eyes of 76 patients, In all but two eye, IOP could be lowered to the normal range
group (A), 40 eyes; group (B), 40 eyes, who received an with topical medication during the follow-up period, without
intravitreal injectionof 4mg triamcinolone acetonide and had development of glaucoma tousoptic nerve head changes.
a follow-up time of 1 weeks interval for 6 weeks. In group
(B), topical prednisolone acetate (0.1%) was administrated 3 Conclusions: After intravitreal injections of 4mg oftriam-
times daily for 2 weeks before injection, and the follow-up cinolone acetonide, an IOP elevation can develop in about
started 1 day before injection. 25% of eyes starting 1 week after injection, but the onset is
inconstant in all cases. In the vast majority, IOP can be
Results: In group (A) IOP increased significantly (p=0.001) normalized by topical medication. Topical steroid administra-
from 13.8 (1.9) mmHg preoperatively to a mean maximum tion pre-injection helped knowing the steroid responders and
of 15.6 (2.7) mmHg postoperatively. An IOP rise to values non-responders, so avoiding the occurrence of 2 ry refractory
higher than 20mmHg was observed in 6 (15%) eyes. Elevation glaucoma steroid-injection.
of IOP occurred 1 week after the injection. In group (B) IOP
increased non significantly (p>0.001) from 14.8 (2.1) mmHg Key Words: Glaucoma – Diabetic macular – Intraocular
preoperatively to a mean maximum of 16.35 (2.7) mmHg injection – Triamcinolone acetonide.
410
519
496 626 557 418 316
488
365
A
316
376
297 337 325 389 329
399
364
B
Fluorescein angiography and optical coherence tomography (OCT) before (A), and OCT 6 weeks after intravitreal injection
of triamcinolone acetonide (B). Note: Central corneal thickness before (557 µ ) and after (325 µ ).
Correspondence to: Dr. Hossam El-Din Khalil,
The Department of Ophthalmology, Beni-Swif University
147
148 Intraocular Pressure Changes after Triamcinolone Acetonide Intravitreal Injection
Introduction lower intraocular concentrations of steroids than
if the steroids were injected intravitreally, we aimed
INJECTION Intravitreal triamcinolone acetonide to evaluate the response of IOP after the intravitreal
has increasingly been used in previous studies as injection of corticosteroids. As well as the IOP
treatment for intraocular proliferative, edematous, changes when the intravitreal triamcinolone ace-
and neovascular diseases, such as central retinal tonide injection is preceded by administration of
vein occlusion, neovascular glaucoma without or topical steroid as a provocative test.
with cataract surgery, chronic pre-phthisical ocular
hypotony, chronic uveitis, persistent pseudophakic Patients and Methods
cystoid macular edema, exudative age-related
macular degeneration, proliferative diabetic retin- Patients were selected outpatient Cairo and
opathy, ischemic ophthalmopathy, sympathetic Beni-Swif Universities from 2010-2011.
ophthalmia, and in other clinical situations [1] .
Direct intraocular injection of steroids delivers the The prospective interventional case series study
desired drug to its target tissue in the most direct included 76 patients (80 eyes) divided into 2 groups.
fashion without extraocular side effects as that Group A included 36 patients (40 eyes) (22 women,
happened after oral steroids administration. After 18 men; 16 right eyes, 24 left eyes) who consecu-
a single intravitreal injection of triamcinolone tively received an intravitreal injection of 4mg
acetonide, one can deliver a concentration of thou- triamcinolone acetonide with topical anaesthesia,
sands of nanograms of triamcinolone to the vitreous and who had a follow-up time of 6 weeks. Group
cavity. Drug concentrations rapidly decrease and B included 40 patients (40 eyes) (24 women, 16
are followed by a subsequent prolonged rate of men; 22 right eyes, 18 left eyes) who consecutively
elimination. A measurable concentration is main- received topical prednisolone acetate (0.1%) 3
tained in the vitreous humor for approximately 90 times daily for 2 weeks as a provocative testprior
days [2] . to triamcinolone acetonide intravitreal injection.
The reasonfor the intravitreal injection of triamci-
Side effects reported so far include cataract; nolone acetonide were progressive decrease of
secondary ocular hypertension leading in some visual acuity due to exudative agerelated macular
patients to secondary chronic open-angle glaucoma; degeneration with subfoveal neovascularization
and post injection, infectious, or sterile endoph- (n=11 eyes), or diffuse diabetic macular oedema
thalmitis [1] . Previous studies have shown that one (n=68 eyes) or Retinal vein occlusion (1 eye).
of the most common side effects of intravitreal Mean age was 50.4 (9.5) years (range 20.1-65.1
triamcinolone acetonide was a steroid-induced years). All patients were fully informed about the
elevation of IOP [3] . Since previous studies exam- experimental character of thetherapy. All patients
ined the rate and amount of elevation of IOP after signed an informed consent. The ethicscommittee
topical application of cortisone leading to much of the university had approved the study.
Fluorescein angiography and optical coherence tomography before (A-C), and 6 weeks after (B-D) intravitreal injection
of triamcinolone acetonide. Note: Decrease in fluorescein leakage and decrease in retinal thickening.Hossam E. Khali, et al. 149
Patients received an intravitreal injection of of the retina, such as diffuse diabetic macular
4mg of crystalline triamcinolone acetonide under oedema and persistent cystoid macular oedema
sterile conditions in the operating theatre. The due to various other diseases, and chronic intraoc-
solution was prepared by the hospital’s pharmacy ular inflammation are some of the leading causes
removing the solvent agent. Using the operation of impaired vision. The intraocular proliferation
microscope, the injection was transconjunctivally of cells is often accompanied and stimulated by
carried out under topical anaesthesia after a para- intraocular inflammation, and macular oedema can
centesis had been performed to decrease the volume be caused by a damaged blood-retinal barrier due
of the globe. Using applanation tonometry, IOP to capillary leakage. Corticosteroids have long
was determined before, and in intervals of 1 week been known to tighten up blood vessels resulting
after the injectionfor 1 month. in a decrease of vessel leakage and, depending on
the concentration, to suppress proliferation of cells.
For inter individual comparisons, only one Consequently, steroids have been used for the
randomly selected eye per patient was taken for treatment of various ocular diseases, applied either
statistical analysis. For intra individual bilateral topically or systemically. Often, however, the
comparison, the four patients with both eyes treated intraocular concentrations of corticosteroids were
were included in the analysis. not sufficiently high, or the systemic side effects
Results were too serious, to effectively treat the ocular
disorder.
In group A, IOP increased significantly
(p150 Intraocular Pressure Changes after Triamcinolone Acetonide Intravitreal Injection
about 25% of the eyes treated. A predictive factor edema: Preliminary results of a prospective controlled
for the rise of IOP may have been the presence of trial. Ophthalmology, 111: 218-225, 2004.
glaucoma before the injection. This relation, how- 4- GRAHAM R.O. and PEYMAN G.A.: Intravitreal injection
ever, was statistically not significant. of dexamethasone. Treatment of experimentally induced
endophthalmitis. Arch. Ophthalmol., 92: 149-54, 1974.
But a statistically significant relation was found 5- TANO Y., SUGITA G., ABRAMS G., et al.: Inhibition
for the younger age with a post-injection rise in of intraocular proliferation with intravitreal corticosteroid.
IOP. Other parameters, such as sex and refractive Am. J. Ophthalmol., 89: 131-6, 1980.
error of the patient did not show a marked influence 6- TANO Y., CHANDLER D. and MACHEMER R.: Treat-
on frequency and amount of the elevation of IOP. ment of intraocular proliferation with intravitreal injection
Interestingly, the presence of diabetes mellitus did of tramcinolone acetonide. Am. J. Ophthalmol., 90: 810-
16, 1980.
not demonstrate a marked influence on the rate of
a postoperative elevation of IOP. From a clinical 7- GILES C.L.: Bulbar perforation during periocular injection
of corticosteroids. Am. J. Ophthalmol., 77: 438-41, 1974.
point of view it may be important that in all but
one eye, the IOP could be controlled by topical 8- McLEAN E.B.: Inadvertent injection of corticosteroid
into the choroidal vasculature. Am. J. Ophthalmol., 80:
antiglaucomatous treatment. Also, as to be expect- 835-7, 1975.
ed, both eyes of the same patient reacted in a
similar way, if both eyes received an intravitreal 9- McCUEN B.W. 2D., BESSLER M., TANO Y., et al.: The
lack of toxicity of intravitreally administered triamcinolone
injection. acetonide. Am. J. Ophthalmol., 91: 785-8, 1981.
In contrast with other clinical studies reporting 10- HIDA T., CHANDLER D., ARENA J.E., et al.: Experi-
on the intravitreal injection of triamcinolone ace- mental and clinical observations of the intraocular toxicity
of commercial corticosteroid preparations. Am. J. Oph-
tonide, the dosage used in the present investigation thalmol., 101: 190-5, 1986.
was about five times higher (20mg versus 4mg)
11- MACHEMER R., SUGITA G. and TANO Y.: Treatment
[12-16,18,19,24,25,27,28,33-35,36] . Without starting a
of intraocular proliferations with intravitreal steroids.
discussion on the clinical usefulness and necessity Trans Am. OphthalmolSoc., 77: 171-80, 1979.
to use a remarkably higher dosage than in other 12- PENFOLD P., GYORY J., HUNYOR A., et al.: Exudative
studies, the results of the present investigation macular degeneration and intravitreal triamcinolone. A
demonstrate that also with this high dosage of pilot study. Aust. NZ. J. Ophthalmol., 23: 293-8, 1995.
intravitreal triamcinolone acetonide, the steroid 13- MACHEMER R.: Five cases in which a depot steroid
induced elevation in IOP can also be controlled (hydrocortisone acetate and methylprednisolone acetate)
without development of a major damage to the was injected into the eye. Retina., 16: 166-7, 1996.
optic nerve. 14- CHALLA J.K., GILLIES M.C., PENFOLD P.L., et al.:
Exudative macular degeneration and intravitreal triamci-
In conclusion, the data of the present study nolone: 18 month follow-up. Aust. NZ. J. Ophthalmol.,
suggest that the intravitreal injection of triamcino- 26: 277-81, 1998.
lone acetonide in a dosage of 20mg leads to a 15- WINGATE R.J. and BEAUMONT P.E.: Intravitreal tri-
secondary ocular hypertension in about 25% of amcinolone and elevated intra ocular pressure. Aust. NZ.
the eyes treated; that the rise of IOP can usually J. Ophthalmol., 27: 431-2, 1999.
be controlled by topical antiglaucomatous medica- 16- JAFFE G.J., BEN-NUN J., GUO H., et al.: Fluocinolo-
tion. Topical steroid administration pre-injection neacetonide sustained drug delivery device to treat severe
helped knowing steroid responders and non- uveitis. Ophthalmology, 107: 2024-33, 2000.
responders, so avoiding the occurrence of 2 ry 17- JONAS J.B., HAYLER J.K. and PANDA-JONAS S.:
refractory glaucoma. Intravitreal injection of crystalline cortisone as adjunctive
treatment of proliferative vitreoretinopathy. Br. J. Oph-
References thalmol., 84: 1064-7, 2000.
1- JONAS J.B., DEGENRING R.F., KREISSIG I., et al.: 18- DANIS R.P., CIULLA T.A., PRATT L.M., et al.: Intrav-
Intraocular pressure elevation after intravitreal triamcino- itreal triamcinolone acetonide in exudative age-related
lone acetonideinjection. Ophthalmology, 112: 593-598, macular degeneration. Retina., 20: 244-50, 2000.
2005. 19- KIVILCIM M., PEYMAN G.A., EL-DESSOUKY E.S.,
2- FLORIAN K.P., JUDY M. SIMPSON, et al.: Intravitreal et al.: Retinal toxicity of triamcinolone acetonide in
silicone-filled eyes. Ophthalmic. Surg. Lasers, 31: 474-
triamcinolone for diabetic macular edema that persists
8, 2000.
after laser treatment: Three-monthefficacy and safety
results of a prospective, randomized, doublemasked, 20- JONAS J.B., HAYLER J.K., SÖFKER A., et al.: Regres-
placebo-controlled clinical trial. Ophthalmol., 11: 2044- sion of neovascular iris vessels by intravitreal injection
2049, 2004. of crystalline cortisone. J. Glaucoma, 10: 284-7, 2001.
3- MASSIN P., AUDREN F. and HAOUCHINE B.: Intrav- 21- JONAS J.B., HAYLER J.K., SÖFKER A., et al.: Intrav-
itreal triamcinolone acetonide for diabetic diffuse macular itreal injection of crystalline cortisone as adjunctiveHossam E. Khali, et al. 151
treatment of proliferative diabetic retinopathy. Am. J. 26- REINHARD T. and SUNDMACHER R.: Adjunctive
Ophthalmol., 131: 468-71, 2001. intracameral application of corticosteroids in patients
with endothelial immune reactions after penetrating kerato-
22- JONAS J.B. and SÖFKER A.: Intraocular injection of
plasty. A pilot study. Transpl. Int., 15: 81-8, 2002.
crystalline cortisone as adjunctive treatment of diabetic
macular edema. Am. J. Ophthalmol., 132: 425-7, 2001. 27- GREENBERG P.B., MARTIDIS A., ROGERS A.H., et
al.: Intravitreal triamcinolone acetonide for macular
23- JONAS J.B., HAYLER J.K. and PANDA-JONAS S.:
oedema due to central retinal vein occlusion. Br. J. Oph-
Intravitreal injection of crystalline cortisone as treatment
thalmol., 86: 247-8, 2002.
of pre-phthisical ocular hypotony. Graef. Arch. Clin. Exp.
Ophthalmol., 239: 464-5, 2001. 28- RANSON N.T., DANIS R.P., CIULLA T.A., et al.: Intra-
vitreal triamcinolone in subfoveal recurrence of choroidal
24- ANTCLIFF R.J., SPALTON D.J., STANFORD M.R., et
neovascularisation after laser treatment in macular degen-
al.: Intravitreal triamcinolone for uveitic cystoid macular
eration. Br. J. Ophthalmol., 86: 527-9, 2002.
edema: An optical coherence tomography study. Ophthal-
mology, 108: 765-72, 2001. 29- BECKER B., BRESNICK G., CHEVRETTE L., et al.:
Intraocular pressure and its response to topical corticos-
25- YOUNG S., LARKIN G., BRANLEY M., et al.: Safety
teroids in diabetes. Arch. Ophthalmol., 76: 477-83, 1966.
and efficacy of intravitreal triamcinolone for cystoid
macular edema in uveitis. Clin. Exp. Ophthalmol., 29: 2- 30- BECKER B. and BALLIN N.: Glaucoma and corticosteroid
6, 2001. provocative testing. Arch. Ophthalmol., 74: 621-4, 1965.You can also read
