Patient with open angle glaucoma present as → a 47-year-old African American male presents for an ophthalmic examination. Medical history is significant for hypertension and type II diabetes mellitus. On slit-lamp examination, there is cupping of the optic disc, with a cup-to-disc ratio > 0.6. Tonometry reveals intraocular pressure of 45 mmHg (normal is 8-21 mmHg). Peripheral field vision loss is noted on visual field exam.
Patient with acute angle closure glaucoma will present with → a 60-year-old Asian American woman presents with sudden ocular pain. She reports she was visiting the planetarium when the pain started and when she walked outside she saw halos around the street lights. The pain was so bad that she began to vomit. She reports her vision is decreased. Physical examination reveals conjunctival injection, a cloudy cornea, and pupils
- Impaired aqueous outflow through a diseased trabecular meshwork causing increasing IOP leading to a gradual increase in pressure and progressive peripheral visual field loss
- Open-angle glaucoma is the most common type accounting for 90% of glaucomas in the US
- Pt will likely be African American and be asymptomatic – diagnosed during routine screening. This is an insidious slow process – pt will usually be unaware
- Visual loss in open-angle progresses from peripheral → central = glaucoma
- Visual loss from central → peripheral = macular degeneration
Acute angle closure glaucoma (ophthalmologic emergency)
- Occurs when the iris dilates and pushes against the lens of the eyes, disrupting the flow of aqueous humor into the anterior chamber. The pressure in the posterior chamber then pushes the peripheral iris forward and blocks the angle
- Acute and severe pain, unilateral, decreased visual acuity with headache nausea and vomiting
- Classic triad of injected conjunctiva, cloudy cornea, and fixed dilated pupil
Iritis will present similarly to acute angle-closure glaucoma except look for a small constricted pupil
Diagnosis is confirmed by tonometry demonstrating increased intraocular pressure
- May demonstrate cupping of the optic nerve
All patients should be screened at age 40 - may present for routine fundoscopy with a cup to disk ratio > 0.5 (<0.5 is normal). This is suggestive but not diagnostic of glaucoma so you will progress to the next step which is tonometry
- Perform tonometry (IOP testing): pressure > 21 mmHg is concerning but not diagnostic - proceed to the next step which is peripheral field testing
- Peripheral field testing and optic disc changes confirm the diagnosis in normal pressure glaucoma
Acute Narrow Angle Closure Glaucoma
- IV Acetazolamide: first line agent - decrease IOP by decreasing aqueous humor production
- Topical beta blocker (ex. timolol) reduces IOP without affecting visual acuity
- Miotics/cholinergics (ex. Pilocarpine, Carbachol)
- Peripheral iridotomy (punches a hole in the iris) is the definitive treatment
Chronic Open Angle Glaucoma
- Prostaglandin analogs are 1st line (ex. latanoprost) - increase outflow of aqueous humor
- Topical beta blocker (Timolol) - decrease production of aqueous humor
- Trabeculoplasty - opens trabecular meshwork
|Open-angle glaucoma is characterized by having full access to the trabecular meshwork (an open angle in the anterior chamber of the eye), but issues with aqueous humor flowing through it. There is primary open-angle glaucoma, the most common form, for which the mechanism is unclear. Secondary open-angle glaucoma occurs when WBC's, RBC's and retinal products are unable to be filtered and obstruct aqueous flow.|
|Closed-angle glaucoma can be due to primary causes, where the lens leads to mechanical obstruction of aqueous humor flow, leading to decreased fluid drainage. It can also be due to secondary causes, such as neovascular proliferation over the iris, compromising the angle housing the trabecular meshwork. Chronic disease can be asymptomatic, whereas acute disease is an emergency, and can present with eye pain and blindness along with headache and a rock-hard eye.|
Migraine headache does not present with eye findings.
Temporal arteritis presents with headache and systemic symptoms of fever, myalgias, anorexia, and tenderness over the temporal artery.
Retinal artery occlusion
Retinal artery occlusion presents with sudden, painless, severe loss of vision. There are no systemic symptoms.
Cortical blindness is a rare adverse effect when prescribing salicylates.
Optic atrophy can occur as an adverse effect with lead compounds, amebicides, and MAO inhibitors.
Papilledema can be a side effect to many systemic medications.
Timolol, a beta-antagonist, is used in the treatment of acute angle-closure glaucoma.
Glyburide has no relationship to glaucoma.
Acetazolamide, a carbonic anhydrase inhibitor, may suppress the production of aqueous humor by 40-60% and is used in the emergency treatment of glaucoma.
Migraine headaches have associated unilateral headache and nausea however there would be no pupillary changes.
Episcleritis is an inflammation of the thin layer of connective tissue between the conjunctiva and sclera. Episcleritis resembles conjunctivitis but is a more localized process and discharge is absent.
Acute uveitis is frequently due to systemic disorders associated HLA-B27-related conditions ankylosing spondylitis, reactive arthritis, psoriasis, ulcerative colitis, and Crohn's disease. The pupil is usually small, inflammatory cells and flare within the aqueous are present.
Contact lens use
The major risk from contact lens wear is bacterial, amebic, or fungal corneal infection, potentially a blinding condition. In this condition the eye may appear red, however the cornea would be clear, and the globe would not be tense.
Past sexual contacts
Past sexual contacts would be related to pupillary abnormalities associated with neurosyphilis.
Recent URI symptoms
URI symptoms would be considered when associated with conjunctivitis. Pupil size is normal and is the pupillary light response. Intraocular pressure is normal.
Visualizing halos around street lights