Open-angle glaucoma

Breast Cancer Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Type chapter name here from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Radiation therapy
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Open-angle glaucoma On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Open-angle glaucoma All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Open-angle glaucoma
CDC on Open-angle glaucoma
Open-angle glaucoma in the news
Blogs on Open-angle glaucoma
Directions to Hospitals Treating Type chapter name here
Risk calculators and risk factors for Open-angle glaucoma

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rohan Bir Singh, M.B.B.S.[2]

Historical Perspective

Glaucoma has been known in medicine since Antiquity. In Greek 'glaukos' a word appearing in the works of Homer where it seems to mean a sparkling silver glare. Later the word was used for colours such as sky-blue or green.The word entered ophthalmology when Hippocrates, in his “Aphorisms”, lists among the infirmities of the aged a condition he called “glaucosis” which he associated with “dimness of vision”. The implied meaning is that of a clouded or blue-green hue of the cornea in end stage forms that may result in corneal edema and/or coinciding cataract. The Hippocratic writings make no clear distinction between cataract and glaucoma. Both Classical and Alexandrian Greeks did not recognize the specific disease which we now call glaucoma.

The definition of glaucoma has changed drastically since its introduction around the time of Hippocrates in approximately 400 BC. The first recognition of a disease associated with a rise in intraocular pressure and thus corresponding to what is now known as glaucoma occurred in the Arabian writings, “Book of Hippocratic treatment”, of At-Tabari (10th century). In European writings, it was Richard Bannister (1622), an English oculist and author of the first book of ophthalmology in English, who recognized glaucoma as a disease with four features: increased intraocular pressure, long duration of the disease, the absence of perception of light and the presence of a fixed pupil. However, throughout the 18th century the term glaucoma was still merely a label applied to an inflamed eye wherein the pupil appeared greenish-blue and the visual prognosis was bad, but the tension of the eye was not stressed.

It was only after the careful description by Antoine-Pierre Demours (1818) that the central concept of a rise in intraocular pressure became fully established. G.J. Guthrie (1823) and William McKenzie, a Scottish clinician (1835) confirmed these findings. Donders (1862) described an incapacitating increased eye tension occurring without any inflammatory symptoms as "simple glaucoma". In 1973 Drance provided for the first time the definition of glaucoma as an optic neuropathy caused by increased intraocular pressure and other associated risk factors.

The first patient in the United States federal government's Compassionate Investigational New Drug program, Robert Randall, was afflicted with glaucoma and had successfully fought charges of marijuana cultivation because it was deemed a medical necessity (U.S. v. Randall) in 1976.

Classification

Open-angle Glaucoma
Primary open-angle glaucoma (POAG) (H40.11)	not associated with known ocular or systemic disorders that cause increased resistance to aqueous outflow or damage to optic nerve usually associated with elevated IOP
Normal-tension glaucoma (H40.12)	considered in continuum of POAG; often used when IOP is not elevated
Juvenile open-angle glaucoma	used when open-angle glaucoma diagnosed at young age (typically 10-30 years of age)
Glaucoma suspect (H40.0)	normal optic disc and visual field associated with elevated IOP suspicious optic disc and/or visual field with normal IOP
Secondary open-angle glaucoma	increased resistance to trabecular meshwork outflow associated with other conditions (e.g. pigmentary-, phacolytic-, steroid-induced-) increased posttrabecular resistance to outflow secondary to elevated episcleral venous pressure (e.g. carotid cavernous sinus fistula)

Epidemiology and Demographics

Primary open-angle glaucoma (POAG) poses a significant public health problem. The estimated prevalence of POAG in the United States in individuals older than 40 years is 1.86% (95% confidence interval, 1.75%–1.96%), based on a meta-analysis of population-based studies. Applied to data from the 2000 US census, this percentage translates to nearly 2.22 million Americans affected. The number of POAG patients is estimated to increase by 50%, to 3.36 million in 2020.

The World Health Organization (WHO) undertook an analysis of the literature to estimate the prevalence, incidence, and severity of the different types of glaucoma on a worldwide basis. The data collected predominantly in the late 1980s and early 1990s, it was estimated the global population of persons with high IOP (>21 mm Hg) to be 104.5 million. The incidence of POAG was estimated at 2.4 million persons per year. Blindness prevalence for all types of glaucoma was estimated at more than 8 million persons, with 4 million cases caused by POAG. Glaucoma was theoretically calculated to be responsible for 12.3% of blindness. This makes glaucoma the second leading cause of blindness worldwide, following cataract.

The estimated prevalence varies widely as per different studies population-based samples; the Rotterdam Study (northern European population) showing a prevalence of 0.8% and the Barbados Eye Study (Caribbean population) showing a prevalence of 7% in individuals older than 40 years. In these studies, there is an increase in the prevalence of glaucoma in older individuals, with estimates for persons in the 7th decade being generally 3 to 8 times higher than those for persons in their 4th decade.

Among whites aged 40 years and older, a prevalence of between 1.1% and 2.1% has been reported based on population-based studies performed throughout the world. The prevalence among black persons and Latino persons is up to 4 times higher compared to the prevalence among whites. Black individuals are also at greater risk of blindness from POAG, and this risk increases with age: in persons aged 46–65 years, the likelihood of blindness from POAG is 15 times higher among blacks than that among whites.

Risk Factors

• Age : The risk increases with the increase in age.The visual field defects were 7 times more likely to progress in patients aged 60 years or older than in those younger than 40 years. Although increased lOP with age has been observed in many populations and may account for part of the relationship between age and glaucoma, studies in Japan have shown a relationship between glaucoma and age even with no increase in lOP in the population.
• Race : The prevalence of POAG is 3 to 4 times greater in black persons and Hispanic persons than in non-Hispanic white individuals. Blindness from glaucoma is at least 4 times more common in blacks than in whites. Glaucoma is more likely to be diagnosed at a younger age and likely to be at a more advanced stage at the time of diagnosis in black patients than in white patients.The Baltimore Eye Survey found that the prevalence of glaucoma increases dramatically with age, particularly among black persons, exceeding 11% in those aged 80 years or older.
• Family History: A positive family history is also a risk factor for POAG. The relative risk of POAG is increased approximately 3.7-fold for individuals who have a sibling with POAG.
• Myopia : The evidence supports an association between POAG and myopia. The concurrence of POAG and myopia cause difficulty in diagnosis and management of POAG. There is an increased difficulty in evaluation of the optic disc is particularly complicated in highly myopic eyes that have tilted discs or posterior Staphyloma. The magnification of the disc due to the myopic refractive error interferes with optic disc evaluation. Myopia-related retinal abnormalities can cause visual field defects apart along with glaucoma. High refractive error may also make it difficult to perform accurate perimetric measurement and to interpret visual field abnormalities.
• Diabetes Mellitus : The role of diabetes mellitus in causing POAG is still controversial. Though some studies have found diabetes plays a significant role in the disease, other studies have not found diabetes to be major risk factor.
• Hypertension : The systemic hypertension is associated with a low risk of the presence of glaucoma in younger patients and with an increased risk in older (>65 years) patients. It is considered that with advancing age, the adverse effects of chronic hypertension on the optic nerve microcirculation may lead to the nerve's susceptibility to the development of glaucomatous optic neuropathy. Many studies demonstrate that lower ocular perfusion pressure is a strong risk factor for the development of glaucoma, independent of lOP alone. Some research groups define ocular perfusion pressure as blood pressure (systolic, diastolic, or mean arterial) minus lOP. The overtreatment of systemic hypertension may be a contributing factor to glaucoma progression in some cases and hence, should be avoided.
• Retinal vein occlusion : The patients with central retinal vein occlusion may lead to an elevated lOP and glaucoma. In some case, there may be presentation of preexisting POAG or other types of glaucoma. After CRVO, patients may develop angle-closure glaucoma or, at a later stage, neovascular glaucoma. The comorbidity is due to elevated lOP in susceptible individuals, thus are at risk of developing CRVO.
• Sleep apnea
• Thyroid disorders
• Hypercholesterolemia
• Migraine
• Raynaud Phenomenon

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X Ray | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Medical Therapy | Surgery |

Medical Management of Glaucoma

1. Two decisions arise in choosing an appropriate glaucoma therapy:

   • when to treat
   • how to treat

2. Primary angle-closure and infantile glaucoma are treated as soon as the diagnosis is made.
3. Open-angle glaucoma is treated:

   • when damage to the optic nerve has been demonstrated in the form of progressive pathologic cupping and/or characteristic visual field defects
   • when IOP is elevated to an extent that it is likely to cause damage to the optic nerve.

4. The goal of currently available glaucoma therapy

   • To preserve visual function by lowering IOP below a level that is likely to produce further damage to the nerve.
   • The treatment regimen should have lowest risk, fewest side effects, and least disruption of the patient’s life

5. Target pressure goal

   • Should actually be a range with an upper IOP limit that is unlikely to lead to further damage of the nerve in a given patient
   • The more advanced the glaucomatous process on initial presentation, the lower the target pressure generally needs to be prevent further progression.
   • An initial reduction in the IOP of 20%-30% from baseline is suggested, but those patients who have progressive NTG may require a decrease of at least 30% from baseline.
   • The target pressure range needs to be reassessed or changed as comparisons of IOP fluctuations, optic nerve changes, and/or visual field progression dictate.

6. The anticipated benefits of any therapeutic regimen should justify the risks, and regimens associated with substantial side effects should be reserved for patients with a high probability of eventual severe visual dysfunction.

Case Studies

Case #1