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© Borgis - Postępy Nauk Medycznych 12/2013, s. 874-879
*Iwona Grabska-Liberek, Jacek Kosmala, Piotr Tesla, Kinga Zelek
Jaskra wtórna związana z wiekiem
Age-related secondary glaucoma
Clinic of Ophthalmology, Medical Center of Postgraduate Education, Warszawa
Head of Clinic: Iwona Grabska-Liberek, MD, PhD, assoc. prof.
Streszczenie
Jaskra wtórna jest chorobą o wieloczynnikowej etiopatogenezie, wtórnej – jak wskazuje nazwa – do innych patologii leżących w obrębie narządu wzroku, a także często poza nim. Wiek pacjenta jest niewątpliwie jednym z czynników predysponujących do rozwoju jaskry wtórnej. Wraz z wiekiem wzrasta ryzyko rozwoju chorób ogólnoustrojowych i chorób oczu. Niektóre typy jaskry wtórnej mogą wystąpić u pacjentów niezależnie od wieku, inne są bardziej charakterystyczne dla młodych dorosłych, a jeszcze inne częściej spotykamy u starszych pacjentów. W grupie wiekowej do 40. roku życia najczęściej rozpoznawano jaskrę wtórną do urazów lub zabiegów chirurgicznych. Pacjenci powyżej 40. roku życia rozwijali jaskrę wtórną najczęściej w wyniku patologii soczewki lub neowaskularyzacji. Możemy wyróżnić wiele przyczyn występowania jaskry wtórnej. Powyższy podział przedstawia jedynie najczęstsze jej typy związane z wiekiem. Diagnozując chorego z jaskrą wtórną, warto więc zwrócić uwagę na jego wiek, gdyż może to niekiedy znacznie przyspieszyć diagnostykę i pozwolić na szybsze wdrożenie odpowiedniego leczenia jak również pozwoli uniknąć skomplikowanych operacji obarczonych poważnym rokowaniem.
Summary
Secondary glaucoma is a disease of multifactorial ethiopathogenesis. The word “secondary” indicates that its cause lies in other pathological lesions within the eye or often – outside it. One of the risk factors that predisposes to secondary glaucoma development is the patient’s age. The risk of systemic and eye diseases increases with age. Some types of secondary glaucoma may occur in patients of every age, others are more common in the group of young patients and some of them are only relevant to the group of the oldest ones. In the group of age between 20 and 40 years the most common ethiopathogenesis of secondary glaucoma was trauma and an eye surgery. In the group of patients above 40 years of age the most common reason to develop the secondary glaucoma occur to be the lens pathology, cataracta surgery and the neovascularization. There are presented many typs of secondary glaucoma. During the examination it is worth to consider the age of the patient as it can expedite diagnosis, appropriate treatment and avoid complicated operations with serious risk.
INTRODUCTION
According to the definition by the European Glaucoma Society (EGS), the secondary glaucoma is an elevated intraocular pressure which causes progressive typical glaucomatous optic neuropathy and visual field loss caused by other ophthalmological or extraocular diseases, drugs and treatments (1). Glaucoma, both secondary and primary, is divided into two types – open-angle and closed-angle. What is more, it is possible for one form to gradually convert into the other. Another factor according to which the secondary glaucoma is classified is the cause. We can distinguish several types of glaucoma, e.g. traumatic, uveitic or lens-related. The number of causes of glaucoma makes it impossible to present all of its forms. Therefore, the main area of interest has been the relation between the patient’s age and the occurrence of specific forms of secondary glaucoma.
In a study published by the Indian Journal of Ophthalmology, 2997 patients with suspected glaucoma were examined. The diagnosis was confirmed in 2650 cases and 579 of those patients (21.84%) were diagnosed with secondary glaucoma. The following observations were made during the analysis of the group’s age:
– patients of 0-20 years of age constituted 25%,
– patients of 21-40 years of age constituted 27%,
– patients of 41-61 years of age constituted 30%,
– patients above 60 years of age constituted 18%.
In younger patients (age below 20 years) the secondary glaucoma developed mostly due to some kind of trauma. In the group of age between 21 and 40 years, the development of glaucoma was usually following an eye surgery. Patients of 41-60 years old usually developed secondary glaucoma during the course of neovascularization. In patients above 60 years of age, lens pathology and surgeries (mostly cataract surgery) are regarded as the main causes of secondary glaucoma (2-4).
TRAUMATIC GLAUCOMA
It is a type of secondary glaucoma which can develop at any age but statistically it is observed more often in younger, active persons without any health burdens.
Posttraumatic haemorrhages to the anterior chamber can cause an elevation of the IOP because of erythrocytes blocking the trabeculation (erythroclastic glaucoma). Although most of posttraumatic haemorrhages to the anterior chamber are temporary and not particularly dangerous, sometimes a prolonged and intensive IOP elevation can damage the optic nerve and cause the cornea to be infiltrated with blood. The optic nerve is at risk when an IOP of more than 50 mmHg persists for 2 days. The extent of the haemorrhage to the anterior chamber is a useful prognostic hint regarding visual acuity and risk of complications. If the haemorrhage takes less than half of the anterior chamber then in 4% of cases an IOP elevation will occur, in 22% of cases – complications and the final visual acuity will be > 6/18. A haemorrhage taking more than half of the anterior chamber will cause an IOP elevation in 85% of cases, complications in 78% of cases and final visual acuity > 6/18 in only 28% of cases.
Treatment: hospitalization. IOP lowering drugs. Miotics are to be avoided due to the possibility of pupillary block. Steroids used locally as they lower the inflammatory state and the risk of secondary haemorrhage. Mydriatics lower the risk of a new haemorrhage from the iris and the ciliary body. Surgical removal of blood when:
– IOP > 50 mmHg for 2 days or > 35 mmHg for 7 days,
– in case of early blood infiltration of the cornea as it can lead to its intensive opacification,
– when the anterior chamber is completely filled with blood (4).
Secondary angle recession glaucoma
As a result of a blunt trauma to the eyeball, the anterior part of the ciliary body can be torn (angle recession). Although traits of angle recession are observed in many patients with posttraumatic haemorrhage to the anterior chamber, after 10 years only 6-9% of them will develop glaucoma (angle recession glaucoma). Gonioscopy can show and irregular widening of the ciliary body which can be accompanied by cicatrization and pigment in the area of angle recession. In a cursory examination, angle hyperpigmentation can be erroneously diagnosed as pigmentary glaucoma.
Treatment: The most effective treatment is trabeculectomy with antimetabolites. An artificial filtration fistula can be applied in case of trabeculectomy failure (4).
Ghost cell glaucoma
The ghost cell glaucoma is caused by blocking of the trabecular meshwork by lixiviated erythrocytes which stem from the blood extravasated to the vitreous humour. After losing their haemoglobin, empty, inflexible erythrocytes penetrate the damaged limited membrane of the vitreous humour to the anterior chamber where they settle on the trabecular meshwork. This occurs ca. 3 months after the trauma with haemorrhage in an aphakial eye and sometimes after vitrectomy and cataract removal. A suspension of green-brown coloured cells, visible with slit lamp, appears in the anterior chamber.
Treatment: IOP-lowering drugs, anterior chamber irrigation, vitrectomy in exceptional cases (4).
In patients between 21 and 40 years of age, as mentioned above, the most frequently encountered is a surgery-related glaucoma. An increase in IOP can be observed immediately after the surgery as well as some time after it. There are several causes which can be the reason for IOP increase, namely: pigment dispersion (pigmentary glaucoma), haemorrhage, ghost cell, inflammations, viscoelastic, epithelial ingrowth (1).
PIGMENTARY GLAUCOMA
The IOP elevation is currently thought to be caused by the intratrabecular spaces being clogged by the pigment and by damage to the trabeculation which is secondary to its lowering, collapse and hardening. Pigment dispersion syndrome (PDS) is considered to be the leading cause of its occurrence. It is characterised by a release of pigment granules from the pigment epithelium of the iris and their accumulation in the anterior segment of the eye. The release of pigment is caused by mechanical rubbing of the posterior pigment layer of the iris against small ligaments of the ciliary zonule as a result of an excessive bulging of the iris in its middle area. A possibility exists of certain abnormalities in the very pigment epithelium of the iris which facilitate the release of the pigment molecules. In some people an overly strenuous effort can cause episodes of pigment dispersion accompanied by IOP elevation. In the course of pigment dispersion syndrome, glaucoma usually manifests in 1/3 of patients in aged 30-40 years. Pigment granules are released into the ventricular fluid, move with its current and accumulate in all structures of the anterior chamber including ciliary zonule fibres. A cataract surgery can lead to a release of the pigment and to trabeculation blocking, which causes IOP elevation. The symptoms are similar to glaucoma in the course of PDS: IOP elevation, Krukenberg’s spindle – vertical pigment accumulation on the corneal endothelium, small pigment granules on the iris and lens, iris pigment epithelium atrophy which leads to images of slit-like, radial defects which cause a transillumination effect, and trabeculation hyperpigmentation in gonioscopy.
Treatment: IOP-lowering drugs, laser trabeculoplasty (effects are better in younger patients), laser iridotomy, trabeculectomy (2).
INFLAMMATORY GLAUCOMA
Inflammation and haemorrhage are a frequent consequence of surgical operations. If they occur, they can lead to fibrosis and anatomic changes. Fibrosis is more commonly found in certain patients (e.g. diabetes patients or with history of uveitis), and after using certain types of lenses, such as anterior chamber intraocular lens. The inflammatory glaucoma can develop as a result of various mechanisms such as oedema of the filtration angle structures, dysfunction of endothelial cells in the angle area, trabeculation block by inflammatory cells and fibrin, breakdown of the blood-aqueous humour barrier resulting from prostaglandins activity or by steroid-induced reduction in aqueous humour flow through trabeculation (3-6). Secondary glaucoma is especially common in Fuchs’ iritis syndrome an in chronic inflammation of the anterior segment of the vascular membrane. Most of the cases of anterior inflammation of the vascular membrane can be classified as idiopathic. Presence of corneal precipitates and a constricted pupil suggest that iritis is the cause of elevated IOP. During a gonioscopic examination, delicate sediments in the filtration angle can be observed. Sometimes peripheral anterior and posterior synechiae with iris bombe can form and lead to angle closure.

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Piśmiennictwo
1. European Glaucoma society: Terminology and guidelines for glaucoma. Dogma, 2 ed., Savona, Italy 2003: 78-81, 87-88.
2. Kański JJ: Okulistyka Kliniczna. Wydawnictwo Urban & Partner, 3 wyd. pol., Wrocław 2009: 424- 445.
3. Agarwal HC, Sood NW, Kalva BR et al.: Secondary glaucoma. Indian Ophthalmol 1982; 30: 121-124.
4. Gadia R, Sihota R, Dada T et al.: Current profile of secondary glaucomas. Indian J Ophthalmology 2008; 56: 285-289.
5. Mandal AK, Bhatia PG, Gothwal VK et al.: Safety and efficacy of simultaneous bilateral primary combined trabeculotomy-trabeculectomy for developmental glaucoma. Indian J Ophthalmol 2002; 50: 13-19.
6. Salim S, Scott IU, Fekrat S et al.: Diagnosis and Treatment of Neovascular Glaucoma. The American Academy of Ophthalmology. EyeNet magazine 2006.
7. Basic and Clinical Science Course. Jaskra (BCSC 10). Wydawnictwo Urban & Partner, 1 wyd. pol., Wrocław 2006: 107-154.
8. Song J, Allingham RR: Treating Phacolytic Glaucoma. The American Academy of Ophthalmology. EyeNet magazine 2004.
9. Prajna NV, Ramakuishnan R, Krihnadas R et al.: Lens induced glaucomas – Visual results and risk factors for final visual acuity. Indian J Ophthalmology 1996: 44 149-15 155.
10. Jacob A, Thomas R, Koshi SP et al.: Prevalenc e of primary glaucoma in an urban South Indian population. Indian J Ophthalmology 1998; 46: 81-86.
11. Mandal AK, Bhatia PG, Gothwal VK et al.: Safety and efficacy of simultaneous bilateral primary combined trabeculotomy-trabeculectomy for developmental glaucoma. Indian J Ophthalmology 2002; 50: 13-19.
12. Majka CP, Chall P, Scott IU et al.: Diagnosis and Management of Psedoexfoliation Glaucoma. The American Academy of Ophthalmology. EyeNet magazine 2006.
13. Singh G, Kaur J, Mall S et al.: Phacolytic glaucoma – its treatment by planned extracapsular cataract extraction with posterior chamber intraocular lens implantations. Indian J Ophthalmol 1997; 42: 145-147.
14. Chatterjee A, Milton R, Thyle S et al.: Prevalence and aetiology of cataract in Punjab. BR J Ophthalmol 1982; 66: 35-62.
15. Deteline TS, Jacobi PC, Krieglstein GK et al.: Prognosis of primary ab extemo surgery for primary congenital glaucoma. Br J Ophthalmol 1999; 83: 317-322.
16. Beatty S, Aggarwal RK, David DB: Simultaneus bilateral cataract extraction in the UK. Br J Ophthalmol 1995; 79: 1111-1114.
17. Hoskins HB Jr, Shaffer RN, Hetherington J et al.: Goniotomy vs trabeculotomy. J Pediatr Ophthalmol Strabismus 1984; 21: 153-158.
18. Sharma RG, Verma GL, Singhal B et al.: A divect evaluation of Scheie’s operation with sclerectomy along with lens extraction in lens induced glaucoma. Ind J Ophthalmol 1983; 31: 639-641.
19. Grikin CA, McGwin G Jr, Long C et al.: Glaucoma after ocular confusion. A cohort study of the United States eye injury registry. J Glaucoma 2005; 14: 470-473.
20. Chalam KV: Ocular Pharmacology. [In:] Tripathi RC (ed.): Basic and clinical science course 2002-2003. Section 2: Fundamentals and Principles of Ophthalmology. American Academy of Ophthalmology 2002: 381-450.
otrzymano: 2013-09-22
zaakceptowano do druku: 2013-11-04

Adres do korespondencji:
*Iwona Grabska-Liberek
Clinic of Ophthalmology
Medical Center of Postgraduate Education
Prof. W. Orłowski Independent Public Clinical Hospital
ul. Czerniakowska 231, 00-416 Warszawa
tel./fax: +48 (22) 629-71-09
e-mail: kl.okulistyki@szpital-orlowskiego.pl

Postępy Nauk Medycznych 12/2013
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