Case Study 17
CC: Routine eye exam
The patient, a 61 year-old female retired school teacher, has not had an eye exam in 10 years. She reports no problems with driving, watching TV, computer or reading. She uses over-the-counter readers for close work. She admits to mild eye burning feeling after reading for long periods of time or in the afternoons. She denies any flashes, floaters, pain, redness or double vision.
Past Ocular History:
Presbyopia. No prior eye surgeries, hx of eye trauma, amblyopia or strabismus.
Past Medical History:
Cesarean delivery x 1
Past Family Ocular History:
Cataract surgery in her mother and father. Negative for macular degeneration, glaucoma or blindness.
Denies any recent illness or any new CNS, heart, lungs, GI, skin or joint symptoms.
Visual Acuity (cc):
OD: 21 mmHg
OS: 23 mmHg
Equal, round and reactive to light, no APD
Full OU, no nystagmus
Confrontational Visual Fields:
Full to finger counting OU
Normal, both sides
|Lids and Lashes||Normal OU|
|Cornea||Clear OU; no krukenberg spindle or embryotoxon|
|Anterior Chamber||Deep and quiet OU|
|Iris||Normal, no neovascularization or atrophy|
|Lens||1+ nuclear sclerotic cataracts OU|
|Anterior Vitreous||Clear OU|
Dilated Fundus Examination:
|OD||Clear view, CDR 0.7 with sharp optic disc margins (no obvious rim thinning or disc hemorrhage); flat macula with normal foveal light reflex; normal vessels and peripheral retina|
|OS||Clear view, CDR 0.8 with sharp optic disc margins (no obvious rim thinning or disc hemorrhage); flat macula with normal foveal light reflex; normal vessels and peripheral retina
Gonioscopy: Open angles with minimal pigmentation in the trabecular meshwork, no synechiae OU
Automated visual field test: superior arcuate defect in both eyes
Pachymetry: 560 OD; 551 OS (within normal range)
Primary open-angle glaucoma
This patient is presenting with primary open-angle glaucoma (POAG). The diagnosis is supported by evidence of increased IOP (normal is 8 to 21 mmHg), optic nerve head abnormality, open anterior chamber angle, visual field deficits and no history to suggest a secondary glaucoma (glaucoma due to an identifiable cause). Differential diagnosis would include steroid-induced glaucoma, pigmentary glaucoma, pseudoexfoliation glaucoma, trauma-induced glaucoma or other identifiable causes of glaucoma associated with high intraocular pressure, intermittent angle-closure glaucoma or an optic neuropathy (to explain the optic nerve head changes and visual field defects).
Primary open-angle glaucoma is an optic neuropathy associated with high IOP and a characteristic visual field loss. The primary problem with open-angle glaucoma is a defect in the trabecular meshwork. The normal draining process of the aqueous humor therefore is disrupted, which causes a rise in intraocular pressure (IOP). Months or years later, the increased pressure leads to a thinned, damaged optic disc. This results in vision loss initially in the periphery. Patients may not notice any vision loss for years, as their central vision remains intact. In primary open-angle glaucoma there is no identifiable cause to the IOP elevation or optic nerve head changes and visual field deficits. Risk factors for open angle glaucoma include central corneal thickness measured with pachymetry (risk is increased the thinner the cornea), race, age and family history (10x the risk in siblings of patients with POAG).
Because the condition is asymptomatic until the late stages, it is usually diagnosed in a routine eye exam. It is important to inquire about ocular trauma, systemic steroid use and family history of glaucoma. Typical findings are elevated IOP and increased cup-to-disc ratio (greater than 0.2) on funduscopic exam. A visual field examination shows defects that are consistent with the state of the optic nerve. Measurements of the nerve fiber layer over the optic nerve can confirm an abnormally thin nerve.
Topical medications are used as first-line therapy to decrease the
intraocular pressure (the only modifiable risk factor). Medication categories include prostaglandins, adrenergics agonists, beta blockers, and carbonic anhydrase inhibitors. The target is a 30% reduction of the baseline intraocular pressure (ideally an IOP of less than 21 mmHg). Other options for treatment include, among others, argon laser trabeculoplasty, trabeculectomy or a tube shunt procedure. The purpose of these treatments is to increase aqueous outflow from the anterior chamber, lowering the intraocular pressure. Regular follow-up with IOP monitoring, visual field assessment and optic nerve examination are important to ensure no glaucoma progression or need to modify therapy.
- What findings are needed for the diagnosis of POAG?
- enlarged cup-to-disc ratio
- visual acuity loss
- family history of glaucoma
- african american race
- What are the consequences of untreated POAG disease?
- loss of central visual acuity
- shallowing of the anterior chamber angle
- thinning of the optic nerve cup-to-disc space
- corneal endothelial cell loss
- What is a common risk factors for POAG?
- steroid use
- history of eye trauma
- congenital iris malformation
1. What findings are needed for the diagnosis of POAG?
a. enlarged cup-to-disc ratio
Patients with primary open angle glaucoma usually have an enlarged cup-to-disc ratio, which signifies loss of optic nerve tissue.
2. What are the consequences of untreated POAG disease?
c. thinning of the optic nerve cup-to-disc space
If untreated, patients with POAG will have continued loss of nerves and enlargement of the optic nerve cup-to-disc ratio.
3. What is a common risk factors for POAG?
The other answers are risk factors for development of: steroid-induced glaucoma, trauma-induced glaucoma, or congenital glaucoma.
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