Morphallaxia-like ocular histology after intravitreal triamcinolone acetonide
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《英国眼科学杂志》
1 Department of Ophthalmology, Faculty of Clinical Medicine Mannheim, Ruperto-Carola-University Heidelberg, Germany
2 Department of Pathology, Faculty of Clinical Medicine Mannheim, Ruperto-Carola-University Heidelberg, Germany
Correspondence to:
Dr J Jonas
Universit?ts-Augenklinik, Theodor-Kutzer-Ufer 1–3, 68167 Mannheim, Germany; Jost.Jonas@augen.ma.uni-heidelberg.de
Accepted for publication 24 September 2003
Keywords: triamcinolone acetonide; infectious endophthalmitis; age related macular degeneration; diabetic macular oedema; cataract surgery
Subretinal or retinal neovascularisation, intravitreal proliferation of non-vascular cells, intraretinal or subretinal oedema, and chronic ocular hypotony have recently been treated by intravitreal injections of steroids such as triamcinolone acetonide.1–3 The diseases included long standing macular oedema due to central retinal vein occlusion, diffuse diabetic macular oedema, exudative age related macular degeneration, proliferative diabetic retinopathy, neovascular glaucoma, proliferative vitreoretinopathy, chronic pre-phthisical ocular hypotony, chronic uveitis, persistent pseudophakic cystoid macular oedema, and other clinical conditions.1–3 Systemic or local side effects reported so far include cataract, secondary ocular hypertension leading in some patients to secondary chronic open angle glaucoma, non-infectious endophthalmitis or "pseudo-endophthalmitis," and post-injection infectious endophthalmitis.4–6 Safety and toxicity investigations have not revealed a negative effect of intravitreal corticosteroids on intraocular structures, yet. Besides a recent report, other histological examinations of globes after intravitreal injections of triamcinolone acetonide in patients have been lacking so far.7 It was, therefore, the purpose of the present report to describe pathohistological findings after an intravitreal injection of triamcinolone acetonide.
Case report
An 86 year old patient received an intravitreal injection of triamcinolone acetonide as treatment for exudative age related macular degeneration in her left eye. Visual acuity was 0.10 left eye, and hand movement right eye. After returning home, she fell hitting her head and eye against a heating apparatus 1 week after the injection. Two days later, she was found lying on the floor almost unconscious. A paralimbal corneal wound corresponding to a former cataract surgery was widely open, and clinical signs of endophthalmitis were present. Since the patient did not perceive any light in her left eye, the eye was enucleated and fixed in a solution of 4% formaldehyde. The globe was prepared in a routine manner for light microscopic examination. An anterior-posterior segment going through the pupil and the optic nerve was cut out of the fixed globe. The segment was dehydrated in alcohol, embedded in paraffin, sectioned for light microscopy, and stained by the periodic acid Schiff (PAS) method.
Histology showed a marked destruction of the whole globe. The paralimbal sclerocorneal incision dating back to the previous cataract surgery was ruptured. Intraocular tissue such as iris, ciliary body, and retina, were markedly destroyed with pronounced loss of cell nuclei and melanin. The blood vessels were widely dilated, filled with erythrocytes, and showed thrombotic signs. The most striking finding was that some areas showed massive infiltration by granulocytes, while other areas were almost completely devoid of inflammatory cells (figs 1 and 2). There was a sharp demarcation line between both areas. In some areas, the outer layers of the sclera showed a dense concentration of inflammatory cells which were sharply demarcated from the inner sclera layers in which almost no granulocytes were detectable. Gram staining did not reveal Gram positive or negative bacteria.
Figure 1 Histological slide showing marked granulocytic infiltration sharply demarcated from areas almost without any infiltration by inflammatory cells. Staining by the periodic acid Schiff method.
Figure 2 Histological slide showing marked granulocytic infiltration sharply demarcated from areas almost without any infiltration by inflammatory cells. Staining by the periodic acid Schiff method.
Comment
The globe presented in this report showed a Morphallaxia-like histology in which a dense infiltration of granulocytes was sharply demarcated by tissue areas in which inflammatory cells were almost completely missing. Such a histology, normally characteristic of demarcation and destruction of necrotic anaemic tissue like intrauterine resorption of a dead fetus, may be explained by the intraocular presence of high concentrations of triamcinolone acetonide. As a steroid, it may have inhibited the immigration of granulocytes into those areas in which the triamcinolone acetonide crystals had not been rinsed out of the eye through the traumatically opened cataract surgery wound. Morphallaxia-like histology is not commonly found in globes enucleated because of infectious endophthalmitis, which is normally characterised by a marked destruction of all intraocular structures with dense infiltration of all ocular structures by inflammatory cells. The Morphallaxia-like morphology of infectious endophthalmitis in eyes with intravitreal triamcinolone acetonide may be paralleled by the clinical observation that patients with infectious endophthalmitis after an intravitreal injection of triamcinolone acetonide usually show almost no pain, which is uncommon for infectious endophthalmitis in eyes without intraocular steroids. The lack of inflammatory cells migrated into the eye may be the histological correlate of the clinical observation.
References
Machemer R, Sugita G, Tano Y. Treatment of intraocular proliferations with intravitreal steroids. Trans Am Ophthalmol Soc 1979;77:171–80.
Penfold PL, Gyory JF, Hunyor AB, et al. Exudative macular degeneration and intravitreal trimcinolone. Aust NZ J Ophthalmol 1995;23:293–8.
Martidis A, Duker JS, Greenberg PB, et al. Intravitreal triamcinolone for refractory diabetic macular edema. Ophthalmology 2002;109:920–7.
Wingate RJ, Beaumont PE. Intravitreal triamcinolone and elevated intraocular pressure. Aust N Z J Ophthalmol 1999;27:431–2.
Sutter FK, Gillies MC. Pseudo-endophthalmitis after intravitreal injection of triamcinolone. Br J Ophthalmol 2003;87:972–4.
Roth DB, Chieh J, Spirn MJ, et al. Noninfectious endophthalmitis associated with intravitreal triamcinolone injection. Arch Ophthalmol 2003;121:1279–82.
Benz MS, Murray TG, Dubovy SR, et al. Endophthalmitis caused by Mycobacterium chelonae abscessus after intravitreal injection of triamcinolone. Arch Ophthalmol 2003;121:271–3.(J B Jonas1 and U Bleyl2)
2 Department of Pathology, Faculty of Clinical Medicine Mannheim, Ruperto-Carola-University Heidelberg, Germany
Correspondence to:
Dr J Jonas
Universit?ts-Augenklinik, Theodor-Kutzer-Ufer 1–3, 68167 Mannheim, Germany; Jost.Jonas@augen.ma.uni-heidelberg.de
Accepted for publication 24 September 2003
Keywords: triamcinolone acetonide; infectious endophthalmitis; age related macular degeneration; diabetic macular oedema; cataract surgery
Subretinal or retinal neovascularisation, intravitreal proliferation of non-vascular cells, intraretinal or subretinal oedema, and chronic ocular hypotony have recently been treated by intravitreal injections of steroids such as triamcinolone acetonide.1–3 The diseases included long standing macular oedema due to central retinal vein occlusion, diffuse diabetic macular oedema, exudative age related macular degeneration, proliferative diabetic retinopathy, neovascular glaucoma, proliferative vitreoretinopathy, chronic pre-phthisical ocular hypotony, chronic uveitis, persistent pseudophakic cystoid macular oedema, and other clinical conditions.1–3 Systemic or local side effects reported so far include cataract, secondary ocular hypertension leading in some patients to secondary chronic open angle glaucoma, non-infectious endophthalmitis or "pseudo-endophthalmitis," and post-injection infectious endophthalmitis.4–6 Safety and toxicity investigations have not revealed a negative effect of intravitreal corticosteroids on intraocular structures, yet. Besides a recent report, other histological examinations of globes after intravitreal injections of triamcinolone acetonide in patients have been lacking so far.7 It was, therefore, the purpose of the present report to describe pathohistological findings after an intravitreal injection of triamcinolone acetonide.
Case report
An 86 year old patient received an intravitreal injection of triamcinolone acetonide as treatment for exudative age related macular degeneration in her left eye. Visual acuity was 0.10 left eye, and hand movement right eye. After returning home, she fell hitting her head and eye against a heating apparatus 1 week after the injection. Two days later, she was found lying on the floor almost unconscious. A paralimbal corneal wound corresponding to a former cataract surgery was widely open, and clinical signs of endophthalmitis were present. Since the patient did not perceive any light in her left eye, the eye was enucleated and fixed in a solution of 4% formaldehyde. The globe was prepared in a routine manner for light microscopic examination. An anterior-posterior segment going through the pupil and the optic nerve was cut out of the fixed globe. The segment was dehydrated in alcohol, embedded in paraffin, sectioned for light microscopy, and stained by the periodic acid Schiff (PAS) method.
Histology showed a marked destruction of the whole globe. The paralimbal sclerocorneal incision dating back to the previous cataract surgery was ruptured. Intraocular tissue such as iris, ciliary body, and retina, were markedly destroyed with pronounced loss of cell nuclei and melanin. The blood vessels were widely dilated, filled with erythrocytes, and showed thrombotic signs. The most striking finding was that some areas showed massive infiltration by granulocytes, while other areas were almost completely devoid of inflammatory cells (figs 1 and 2). There was a sharp demarcation line between both areas. In some areas, the outer layers of the sclera showed a dense concentration of inflammatory cells which were sharply demarcated from the inner sclera layers in which almost no granulocytes were detectable. Gram staining did not reveal Gram positive or negative bacteria.
Figure 1 Histological slide showing marked granulocytic infiltration sharply demarcated from areas almost without any infiltration by inflammatory cells. Staining by the periodic acid Schiff method.
Figure 2 Histological slide showing marked granulocytic infiltration sharply demarcated from areas almost without any infiltration by inflammatory cells. Staining by the periodic acid Schiff method.
Comment
The globe presented in this report showed a Morphallaxia-like histology in which a dense infiltration of granulocytes was sharply demarcated by tissue areas in which inflammatory cells were almost completely missing. Such a histology, normally characteristic of demarcation and destruction of necrotic anaemic tissue like intrauterine resorption of a dead fetus, may be explained by the intraocular presence of high concentrations of triamcinolone acetonide. As a steroid, it may have inhibited the immigration of granulocytes into those areas in which the triamcinolone acetonide crystals had not been rinsed out of the eye through the traumatically opened cataract surgery wound. Morphallaxia-like histology is not commonly found in globes enucleated because of infectious endophthalmitis, which is normally characterised by a marked destruction of all intraocular structures with dense infiltration of all ocular structures by inflammatory cells. The Morphallaxia-like morphology of infectious endophthalmitis in eyes with intravitreal triamcinolone acetonide may be paralleled by the clinical observation that patients with infectious endophthalmitis after an intravitreal injection of triamcinolone acetonide usually show almost no pain, which is uncommon for infectious endophthalmitis in eyes without intraocular steroids. The lack of inflammatory cells migrated into the eye may be the histological correlate of the clinical observation.
References
Machemer R, Sugita G, Tano Y. Treatment of intraocular proliferations with intravitreal steroids. Trans Am Ophthalmol Soc 1979;77:171–80.
Penfold PL, Gyory JF, Hunyor AB, et al. Exudative macular degeneration and intravitreal trimcinolone. Aust NZ J Ophthalmol 1995;23:293–8.
Martidis A, Duker JS, Greenberg PB, et al. Intravitreal triamcinolone for refractory diabetic macular edema. Ophthalmology 2002;109:920–7.
Wingate RJ, Beaumont PE. Intravitreal triamcinolone and elevated intraocular pressure. Aust N Z J Ophthalmol 1999;27:431–2.
Sutter FK, Gillies MC. Pseudo-endophthalmitis after intravitreal injection of triamcinolone. Br J Ophthalmol 2003;87:972–4.
Roth DB, Chieh J, Spirn MJ, et al. Noninfectious endophthalmitis associated with intravitreal triamcinolone injection. Arch Ophthalmol 2003;121:1279–82.
Benz MS, Murray TG, Dubovy SR, et al. Endophthalmitis caused by Mycobacterium chelonae abscessus after intravitreal injection of triamcinolone. Arch Ophthalmol 2003;121:271–3.(J B Jonas1 and U Bleyl2)