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]

Overview

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)