Glaucoma natural history, complications and prognosis: Difference between revisions
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== Overview == | |||
==Natural History and Prognosis of Open Angle Glaucoma== | ==Natural History and Prognosis of Open Angle Glaucoma== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Rohan Bir Singh, M.B.B.S.[2]..
Overview
Natural History and Prognosis of Open Angle Glaucoma
The absence of symptoms in open angle glaucoma (OAG) causes delay in the timely detection and diagnosis of the disease. Usually before the patient presents with first symptoms, severe and irreversible damage has usually occurred to the visual field in one or both eyes. The rate of prognosis of the visual field defect varies from patient to patient, and treatment of the glaucoma does not completely halt the visual field loss and the deterioration in the visual field progresses despite aggressive therapy.[1]
The incidence of blindness 20 years after the initial diagnosis of OAG has been estimated at 27% for one eye and 9% for both eyes in a primarily Caucasian population.[2] There are multiple studies covering people of various ethnicities that have found the mean change in visual field testing for European-derived, Hispanic, African-derived and Chinese was –1.12, –1.26, –1.33 and –1.56 dB/year, respectively.[3]
The Ocular Hypertension Treatment Study (OHTS) shows that the after 5 years of regular follow-up, progression of OAG from ocular hypertension was 4.4% in the treated group in comparison to 9.5% in the untreated group.However, over 90% of the untreated subjects did not develop visual field or disc changes consistent with OAG.[4]
The Collaborative Normal Tension Glaucoma Study (CNTGS) studied the natural course of untreated NTG.[5] The study specifically focused on patients with glaucomatous optic nerve damage and visual field loss accompanied by IOP in the normal range. It is believed that NTG represents a distinct variety of glaucoma from primary OAG, the two represent a continuum of glaucomas. At 5–7 years of follow-up, the progression of the visual field defect increases to 60% of those individuals with untreated glaucoma with optic nerve damage, visual loss and IOP under 21 mmHg. The treatment targeting IOP lowering of >30% decreased the progression rate to 20%. Most cases progressed slowly, requiring several years to demonstrate progression; in other cases, deterioration manifested within 1 year. The mean estimated slope of the MD index deterioration for all untreated subjects was –0.41 dB/year. However, the MD index ranged from –0.2 dB/year to –2 dB or more/year. This 10-fold range reflects the broad range in the rates of deterioration.[6]
Natural History and Prognosis of Angle Closure Glaucoma
ACG is characterized by apposition of the peripheral iris against the trabecular meshwork, thus resulting in obstruction of the aqueous outflow. The main mechanisms of closure are pupillary block, plateau iris, lens-related and retrolenticular causes.
ACG may be divided into acute, subacute and chronic ACG. All the three types have varied clinical manifestations, but they can still occur at different times in the same person.
- In acute ACG, closure of the angle occurs suddenly, resulting in rapid rise in IOP. The affected person presents with dramatic symptoms i.e. severe ocular pain, nausea, vomiting, headache and blurred vision.
- Subacute or intermittent ACG occurs when episodes of pupillary block resolve spontaneously and can recur repeatedly over time.
- Chronic ACG develops when the angle narrows slowly and results in scarring between the peripheral iris and the trabecular meshwork.
The natural history of ACG has been subdivided into three stages:
- an anatomically narrow angle without elevated IOP, abnormal visual fields or peripheral anterior synechia.
- development of peripheral anterior synechia or a closed angle with elevated IOP.
- development of an anatomical angle closure with glaucomatous optic nerve and visual field changes, termed primary angle closure glaucoma.
The prevalence and pattern of disease varies across different parts of the world. The majority of patients with ACG are Asian due to their anatomical predisposition.[7]
The first-line treatment of LPI relieves the relative pupillary block element. The response to LPI and the long-term course of PACG appears to vary by race. Studies found that LPI in Caucasian subjects with ACG were more likely to effectively prevent the subsequent need for surgical intervention than LPI in Asian subjects. Intraocular pressure was controlled with LPI alone in 65–76% of eyes, with only 0–13% of the eyes requiring subsequent filtering surgery.[8] In comparison in Asian populations, the majority of eyes with established ACG required antiglaucoma medications or filtering surgery, despite undergoing treatment with LPI. The disease in Asians appears to be more aggressive. Even after laser iridotomy for eyes with narrow angles, the rates of progression to ACG can be significant. A decade after treatment for acute PAC, 47.8% of the patients developed glaucomatous optic neuropathy.[9] Several years after the initial attack of acute angle closure in Asian subjects, 17.8% were blind in the affected eye and half had blindness caused by the advanced glaucoma. Thus, Asian patients are at a higher risk of further glaucomatous damage even after patent LPI and would benefit from long-term follow-up.[10]
References
- ↑ Oliver, JE; Hattenhauer, MG; Herman, D; Hodge, DO; Kennedy, R; Fang-Yen, M; Johnson, DH (2002). "Blindness and glaucoma: a comparison of patients progressing to blindness from glaucoma with patients maintaining vision". American journal of ophthalmology. 133 (6): 764–72. ISSN 0002-9394. PMID 12036667.
- ↑ Hattenhauer, Matthew G; Johnson, Douglas H; Ing, Helen H; Herman, David C; Hodge, David O; Yawn, Barbara P; Butterfield, Linda C; Gray, Darryl T (1998). "The probability of blindness from open-angle glaucoma". Ophthalmology. Elsevier BV. 105 (11): 2099–2104. doi:10.1016/s0161-6420(98)91133-2. ISSN 0161-6420. PMID 9818612.
- ↑ Broman, Aimee Teo; Quigley, Harry A.; West, Sheila K.; Katz, Joanne; Munoz, Beatriz; Bandeen-Roche, Karen; Tielsch, James M.; Friedman, David S.; Crowston, Jonathan; Taylor, Hugh R.; Varma, Rohit; Leske, M. Cristina; Bengtsson, Boel; Heijl, Anders; He, Mingguang; Foster, Paul J. (2008-01-01). "Estimating the Rate of Progressive Visual Field Damage in Those with Open-Angle Glaucoma, from Cross-Sectional Data". Investigative ophthalmology & visual science. Association for Research in Vision and Ophthalmology (ARVO). 49 (1): 66. doi:10.1167/iovs.07-0866. ISSN 1552-5783. PMC 224630939875 Check
|pmc=value (help). PMID 18172076. - ↑ Template:Cite
- ↑ Template:Cite
- ↑ Anderson, DR (2003). "Collaborative normal tension glaucoma study". Current opinion in ophthalmology. 14 (2): 86–90. ISSN 1040-8738. PMID 12698048.
- ↑ Thomas, R; Parikh, R; Muliyil, J; Kumar, RS (2003). "Five-year risk of progression of primary angle closure to primary angle closure glaucoma: a population-based study". Acta ophthalmologica Scandinavica. 81 (5): 480–5. ISSN 1395-3907. PMID 14510795.
- ↑ Robin, AL; Pollack, IP (1982). "Argon laser peripheral iridotomies in the treatment of primary angle closure glaucoma. Long-term follow-up". Archives of ophthalmology (Chicago, Ill. : 1960). 100 (6): 919–23. ISSN 0003-9950. PMID 7092629.
- ↑ Alsagoff, Z; Aung, T; Ang, LP; Chew, PT (2000). "Long-term clinical course of primary angle-closure glaucoma in an Asian population". Ophthalmology. 107 (12): 2300–4. ISSN 0161-6420. PMID 11097612.
- ↑ Aung, Tin; Friedman, David S; Chew, Paul T.K; Ang, Leonard P; Gazzard, Gus; Lai, Yoke-Fong; Yip, Leonard; Lai, Hong; Quigley, Harry; Seah, Steve K.L (2004). "Long-term outcomes in asians after acute primary angle closure". Ophthalmology. Elsevier BV. 111 (8): 1464–1469. doi:10.1016/j.ophtha.2003.12.061. ISSN 0161-6420. PMID 15288972.