Publication details
Primární či sekundární glaukom? – kasuistika.
| Title in English | Primary or secondary glaucoma: a clinical case report. |
|---|---|
| Authors | |
| Year of publication | 2010 |
| Type | Article in Proceedings |
| Conference | Sborník abstrakt, Kongres České glaukomové společnosti. |
| MU Faculty or unit | |
| Citation | |
| Field | ORL, ophthalmology, stomatology |
| Keywords | Primary glaucoma; secondary glaucoma; clinical case report; episcleritis; orbital myositis |
| Description | Objective: To present the clinical case report with elevated intraocular pressure of the left eye in a patient with chronic open-angle glaucoma with suspected secondary component. Past history: A 58-year-old male has been treated for POAG since 1982. His right eye underwent trabeculectomy twice (1991, 2003). IOP has been compensated up to 16 mmHg in both eyes since 2003 (chronic therapy: both eyes Xalatan, left eye Trusopt). History of present illness: On follow-up in April 2009 patient came with signs of episcleritis and elevated IOP up to 45 mmHg in the left eye. There was seen preseptal edema of both eyelids imitating proptosis, which was not confirmed by exophthalmometry. Thickened extraocular muscles were observed by ultrasonography. Endocrinologist excluded thyroid orbitopathy. Immunologist excluded systemic connective tissue diseases. NMR of orbits and brain showed physiological findings, but also accidental finding of left-sided maxillary sinusitis. Therefore otorhinolaryngologist indicated local and systemic antibiotics. Despite local ophthalmic antibiotics, corticosteroids and maximal antiglaucomatous therapy IOP still was raised up to 40 mmHg. Therefore patient underwent trabeculectomy in the left eye. Conclusion: Authors present a case of patient with long history of POAG and sudden IOP elevation on the left eye with signs of episcleritis and thickened extraocular muscles. Thyroid orbitopathy and systemic connective tissue diseases were excluded. Three months after surgery IOP is well compensated up to 16 mmHg with beta-blockers, without inflammatory signs. The question still remains. IOP elevation was caused by component of secondary glaucoma within episcleritis, myositis and trabeculitis probably in connection with maxillary sinusitis. Or was it just decompensation of POAG with accidental finding of inflammation in maxillary sinus with secondary orbital myositis? |