Glaucoma natural history, complications and prognosis: Difference between revisions
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==Prognosis== | ==Natural History and Prognosis== | ||
The absence of symptoms in OAG plays a major role in delaying the detection and diagnosis of the disease. By the time of appearance of first symptoms, severe and irreversible damage has usually occurred to the visual field in one or both eyes. The rate of progression of the visual field defect varies in patients, and treatment of the glaucoma may not completely halt the visual field loss and the deterioration in the visual field progresses despite aggressive therapy.<ref name="Oliver Hattenhauer Herman Hodge 2002 pp. 764–72">{{cite journal | last=Oliver | first=JE | last2=Hattenhauer | first2=MG | last3=Herman | first3=D | last4=Hodge | first4=DO | last5=Kennedy | first5=R | last6=Fang-Yen | first6=M | last7=Johnson | first7=DH | title=Blindness and glaucoma: a comparison of patients progressing to blindness from glaucoma with patients maintaining vision. | journal=American journal of ophthalmology | volume=133 | issue=6 | year=2002 | issn=0002-9394 | pmid=12036667 | pages=764–72}}</ref> | |||
The | 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 white population.<ref name="Hattenhauer Johnson Ing Herman 1998 pp. 2099–2104">{{cite journal | last=Hattenhauer | first=Matthew G | last2=Johnson | first2=Douglas H | last3=Ing | first3=Helen H | last4=Herman | first4=David C | last5=Hodge | first5=David O | last6=Yawn | first6=Barbara P | last7=Butterfield | first7=Linda C | last8=Gray | first8=Darryl T | title=The probability of blindness from open-angle glaucoma | journal=Ophthalmology | publisher=Elsevier BV | volume=105 | issue=11 | year=1998 | issn=0161-6420 | pmid=9818612 | doi=10.1016/s0161-6420(98)91133-2 | pages=2099–2104}}</ref> Multiple studies in different social groups 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.<ref name="Broman Quigley West Katz 2008 p=66">{{cite journal | last=Broman | first=Aimee Teo | last2=Quigley | first2=Harry A. | last3=West | first3=Sheila K. | last4=Katz | first4=Joanne | last5=Munoz | first5=Beatriz | last6=Bandeen-Roche | first6=Karen | last7=Tielsch | first7=James M. | last8=Friedman | first8=David S. | last9=Crowston | first9=Jonathan | last10=Taylor | first10=Hugh R. | last11=Varma | first11=Rohit | last12=Leske | first12=M. Cristina | last13=Bengtsson | first13=Boel | last14=Heijl | first14=Anders | last15=He | first15=Mingguang | last16=Foster | first16=Paul J. | title=Estimating the Rate of Progressive Visual Field Damage in Those with Open-Angle Glaucoma, from Cross-Sectional Data | journal=Investigative ophthalmology & visual science | publisher=Association for Research in Vision and Ophthalmology (ARVO) | volume=49 | issue=1 | date=2008-01-01 | issn=1552-5783 | pmid=18172076 | pmc=224630939875 | doi=10.1167/iovs.07-0866 | page=66}}</ref> | ||
The Ocular Hypertension Treatment Study elucidated the natural history of OAG by identifying the rate of conversion from ocular hypertension to primary OAG and the impact of treating IOP (decreasing IOP more than 20% from baseline) on the development of OAG. After 5 years of regular follow-up, conversion to OAG from ocular hypertension was 4.4% in the treated group as compared with 9.5% in the untreated group. Thus, a protective effect of treatment was seen in over half of the patients. However, over 90% of the untreated subjects did not develop visual field or disc changes consistent with OAG during this time.<ref name="Gordon Beiser Brandt Heuer 2002 pp. 714–20; discussion 829–30">{{cite | last=Gordon | first=MO | last2=Beiser | first2=JA | last3=Brandt | first3=JD | last4=Heuer | first4=DK | last5=Higginbotham | first5=EJ | last6=Johnson | first6=CA | last7=Keltner | first7=JL | last8=Miller | first8=JP | last9=Parrish | first9=RK 2nd | last10=Wilson | first10=MR | last11=Kass | first11=MA | title=The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. | journal=Archives of ophthalmology (Chicago, Ill. : 1960) | volume=120 | issue=6 | year=2002 | issn=0003-9950 | pmid=12049575 | pages=714–20; discussion 829–30}}</ref> | |||
This variability in clinical course was also found by the Collaborative Normal Tension Glaucoma Study (CNTGS). CNTGS documented the natural course of untreated NTG.<ref name="American journal of ophthalmology 1998 pp. 498–505">{{cite | title=The effectiveness of intraocular pressure reduction in the treatment of normal-tension glaucoma. Collaborative Normal-Tension Glaucoma Study Group. | journal=American journal of ophthalmology | volume=126 | issue=4 | year=1998 | issn=0002-9394 | pmid=9780094 | pages=498–505}}</ref> The study specifically focused on patients with glaucomatous optic nerve damage and visual field loss accompanied by IOP in the normal range. While some believe that NTG represents a distinct variety of glaucoma from primary OAG, the two most likely represent a continuum of glaucomas. After 5–7 years of follow-up, progression of the visual field defect was noted in 60% of those individuals with untreated glaucoma with optic nerve damage, visual loss and IOP under 21 mmHg. Treatment targeting IOP lowering of >30% decreased the progression rate to 20%.[26] 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. | |||
== Natural History of Angle Closure Glaucoma == | |||
The ACG causes more serious loss of vision than OAG. ACGs are characterized by apposition of the peripheral iris against the trabecular meshwork, resulting in obstruction of the aqueous outflow. The main mechanisms of closure are pupillary block, plateau iris, lens-related and retrolenticular causes. The most common cause is pupillary block. | |||
ACG may be divided into acute, subacute and chronic ACG. Although they represent different clinical manifestations, they can 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 may present with dramatic symptoms of 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: | |||
(1) an anatomically narrow angle without elevated IOP, abnormal visual fields or peripheral anterior synechia (primary angle closure suspect [PAC]), | |||
(2) development of peripheral anterior synechia or a closed angle with elevated IOP, labeled PAC | |||
(3) development of an anatomical angle closure with glaucomatous optic nerve and visual field changes, termed primary angle closure glaucoma (PACG). | |||
Although the prevalence and pattern of disease varies across different parts of the world, the majority of those with ACG will be Asian due to their anatomical predisposition. Data on the natural history of ACG are limited. Large population-based data on the disease progression are nonexistent. In one small study, 22% of the normal patients with narrow angles developed synechial angle closure (64%) or appositional angle closure (36%) over a period of 5 years.<ref name="Thomas Parikh Muliyil Kumar 2003 pp. 480–52">{{cite journal | last=Thomas | first=R | last2=Parikh | first2=R | last3=Muliyil | first3=J | last4=Kumar | first4=RS | title=Five-year risk of progression of primary angle closure to primary angle closure glaucoma: a population-based study. | journal=Acta ophthalmologica Scandinavica | volume=81 | issue=5 | year=2003 | issn=1395-3907 | pmid=14510795 | pages=480–5}}</ref> | |||
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.<ref name="Robin Pollack 1982 pp. 919–23">{{cite journal | last=Robin | first=AL | last2=Pollack | first2=IP | title=Argon laser peripheral iridotomies in the treatment of primary angle closure glaucoma. Long-term follow-up. | journal=Archives of ophthalmology (Chicago, Ill. : 1960) | volume=100 | issue=6 | year=1982 | issn=0003-9950 | pmid=7092629 | pages=919–23}}</ref> 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.<ref name="Alsagoff Aung Ang Chew 2000 pp. 2300–4">{{cite journal | last=Alsagoff | first=Z | last2=Aung | first2=T | last3=Ang | first3=LP | last4=Chew | first4=PT | title=Long-term clinical course of primary angle-closure glaucoma in an Asian population. | journal=Ophthalmology | volume=107 | issue=12 | year=2000 | issn=0161-6420 | pmid=11097612 | pages=2300–4}}</ref> 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.<ref name="Aung Friedman Chew Ang 2004 pp. 1464–1469">{{cite journal | last=Aung | first=Tin | last2=Friedman | first2=David S | last3=Chew | first3=Paul T.K | last4=Ang | first4=Leonard P | last5=Gazzard | first5=Gus | last6=Lai | first6=Yoke-Fong | last7=Yip | first7=Leonard | last8=Lai | first8=Hong | last9=Quigley | first9=Harry | last10=Seah | first10=Steve K.L | title=Long-term outcomes in asians after acute primary angle closure | journal=Ophthalmology | publisher=Elsevier BV | volume=111 | issue=8 | year=2004 | issn=0161-6420 | pmid=15288972 | doi=10.1016/j.ophtha.2003.12.061 | pages=1464–1469}}</ref> | |||
== References == | == References == | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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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]
Natural History and Prognosis
The absence of symptoms in OAG plays a major role in delaying the detection and diagnosis of the disease. By the time of appearance of first symptoms, severe and irreversible damage has usually occurred to the visual field in one or both eyes. The rate of progression of the visual field defect varies in patients, and treatment of the glaucoma may 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 white population.[2] Multiple studies in different social groups 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 elucidated the natural history of OAG by identifying the rate of conversion from ocular hypertension to primary OAG and the impact of treating IOP (decreasing IOP more than 20% from baseline) on the development of OAG. After 5 years of regular follow-up, conversion to OAG from ocular hypertension was 4.4% in the treated group as compared with 9.5% in the untreated group. Thus, a protective effect of treatment was seen in over half of the patients. However, over 90% of the untreated subjects did not develop visual field or disc changes consistent with OAG during this time.[4]
This variability in clinical course was also found by the Collaborative Normal Tension Glaucoma Study (CNTGS). CNTGS documented 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. While some believe that NTG represents a distinct variety of glaucoma from primary OAG, the two most likely represent a continuum of glaucomas. After 5–7 years of follow-up, progression of the visual field defect was noted in 60% of those individuals with untreated glaucoma with optic nerve damage, visual loss and IOP under 21 mmHg. Treatment targeting IOP lowering of >30% decreased the progression rate to 20%.[26] 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.
Natural History of Angle Closure Glaucoma
The ACG causes more serious loss of vision than OAG. ACGs are characterized by apposition of the peripheral iris against the trabecular meshwork, resulting in obstruction of the aqueous outflow. The main mechanisms of closure are pupillary block, plateau iris, lens-related and retrolenticular causes. The most common cause is pupillary block.
ACG may be divided into acute, subacute and chronic ACG. Although they represent different clinical manifestations, they can 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 may present with dramatic symptoms of 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:
(1) an anatomically narrow angle without elevated IOP, abnormal visual fields or peripheral anterior synechia (primary angle closure suspect [PAC]),
(2) development of peripheral anterior synechia or a closed angle with elevated IOP, labeled PAC
(3) development of an anatomical angle closure with glaucomatous optic nerve and visual field changes, termed primary angle closure glaucoma (PACG).
Although the prevalence and pattern of disease varies across different parts of the world, the majority of those with ACG will be Asian due to their anatomical predisposition. Data on the natural history of ACG are limited. Large population-based data on the disease progression are nonexistent. In one small study, 22% of the normal patients with narrow angles developed synechial angle closure (64%) or appositional angle closure (36%) over a period of 5 years.[6]
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.[7] 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.[8] 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.[9]
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
- ↑ 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.