eMedicine Specialties > Ophthalmology > Intraocular Pressure
Glaucoma, Low Tension: Differential Diagnoses & Workup
Updated: Jun 22, 2006
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Differential Diagnoses
Other Problems to Be Considered
Intermittent IOP elevation
Burned-out glaucoma
Nonglaucomatous optic nerve
Congenital disc anomalies/cupping
Myopia with peripapillary atrophy
Optic nerve coloboma/pit
Vascular etiology
Carotid and ophthalmic artery occlusion
Previous blood loss or shocklike episode
Neurologic etiology
Hereditary optic neuropathy
Leber optic atrophy
Dominant or recessive optic atrophy
Tonometric error (thin cornea)
Workup
Laboratory Studies
- Perform blood tests
- CBC (rule out anemia)
- Erythrocyte sedimentation rate (ESR) rarely is elevated in LTG and typically is obtained in cases of decreased central acuity with a pale nerve to rule out anterior ischemic optic neuropathy (AION).
- Rapid plasma reagent (RPR), fluorescein treponema antibody (FTA)
- Checking for the presence of antinuclear antibody (ANA) is recommended to rule out collagen-vascular and autoimmune diseases. Screening for extractable nuclear antigens (ie, Ro, La, Sm) also is recommended to rule out autoimmune diseases.
- Serum immunofixation for monoclonal gammopathy is indicated. Approximately 10% of patients with LTG have monoclonal gammopathy (paraproteinemia), which represents a benign condition two thirds of the time. However, lymphoproliferative disorders (ie, cancers) need to be ruled out by a hemato-oncology specialist if this test is positive.
- High-sensitivity C reactive protein is becoming the criterion standard for documenting both symptomatic and nonsymptomatic ischemic heart disease and is often positive in patients with LTG.
- Mitochondrial testing for Leber (when indicated)
Imaging Studies
- Optic nerve head and/or retinal nerve fiber analysis may be helpful in diagnosing and monitoring progression of glaucomatous optic neuropathy.
- Analyze optic nerve head with confocal scanning laser ophthalmoscopy (SLO), eg, Heidelberg Retinal Tomograph, or optical coherence topography (OCT).
- Analyze retinal nerve fiber with confocal SLO, OCT, or scanning laser polarimetry (GDx). Often, retinal nerve fiber layer changes may occur before any changes on visual field testing. Most often nerve fiber layer thinning occurs first in the superior and inferior poles.
- Neuroimaging of orbits and head
- MRI is the preferred imaging modality compared to CT scan because of its higher sensitivity.
- Controversy exists as to whether neuroimaging should be performed routinely. Some advocate referral to neuroophthalmology if concerned.
- Neuroimaging should be performed in any case with the following:
- Markedly asymmetric disease
- Increased optic disc pallor relative to cupping
- Unusual visual field defects, particularly those with respect to the vertical midline
- Rapid progression of visual fields
- Rapid progression of optic neuropathies
- Dyschromatopsia
- Afferent papillary defect with mild cupping
- If indicated, carotid Dopplers are recommended to rule out carotid insufficiency.
- When indicated, a chest x-ray is necessary to rule out sarcoidosis.
Other Tests
- To rule out nocturnal hypotension, 24-hour ambulatory blood pressure monitoring is advised.
- Diurnal tension curve: Although IOP may be normal during an examination, the patient may have intermittent spikes in IOP throughout the day that may explain optic nerve and visual field damage.
- Future diagnostic modalities - Ocular blood flow analysis
- SLO - Retinal and choroidal, superficial optic nerve head
- Doppler ultrasound - Carotid arteries
- Confocal scanning laser Doppler flowmetry (Heidelberg Retinal Flowmetry) - Short PCA circulation, optic nerve head
Histologic Findings
Findings include posterior deformation of cribriform plate, with compression of lamina due to direct deformation by secondary vascular compression, resulting in glial atrophy.
More on Glaucoma, Low Tension |
| Overview: Glaucoma, Low Tension |
Differential Diagnoses & Workup: Glaucoma, Low Tension |
| Treatment & Medication: Glaucoma, Low Tension |
| Follow-up: Glaucoma, Low Tension |
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References
Abedin S, Simmons RJ, Grant WM. Progressive low-tension glaucoma: treatment to stop glaucomatous cupping and field loss when these progress despite normal intraocular pressure. Ophthalmology. Jan 1982;89(1):1-6. [Medline].
Fraunfelder FT, Roy FH. Current Ocular Therapy. Philadelphia: WB Saunders;2000: 488-9.
Hitchings RA. Low tension glaucoma--its place in modern glaucoma practice. Br J Ophthalmol. Aug 1992;76(8):494-6. [Medline].
Netland PA, Chaturvedi N, Dreyer EB. Calcium channel blockers in the management of low-tension and open-angle glaucoma. Am J Ophthalmol. May 15 1993;115(5):608-13. [Medline].
Stewart WC, Reid KK. Incidence of systemic and ocular disease that may mimic low-tension glaucoma. J Glaucoma. 1992;1:27-31.
Werner E. Progressive normal-tension glaucoma. I. Analysis. J Glaucoma. Dec 1996;5(6):422-6. [Medline].
Further Reading
Keywords
LTG, low-pressure glaucoma, optic neuropathy, intraocular pressure, primary open-angle glaucoma, POAG
Differential Diagnoses & Workup: Glaucoma, Low Tension