Low-Tension Glaucoma Workup

Updated: Sep 20, 2018
  • Author: Mitchell V Gossman, MD; Chief Editor: Hampton Roy, Sr, MD  more...
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Workup

Laboratory Studies

Blood tests in low-tension glaucoma (LTG) that may be considered depending on the clinical presentation include the following:

  • Order a CBC count to rule out anemia.
  • Erythrocyte sedimentation rate (ESR) rarely is elevated in low-tension glaucoma and typically is obtained in cases of decreased central acuity with a pale nerve to rule out anterior ischemic optic neuropathy (AION) depending on the tempo of vision loss.
  • Order rapid plasma reagent (RPR) and fluorescein treponema antibody (FTA) testing.
  • 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 low-tension glaucoma 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 results from this test are positive.
  • Mitochondrial testing for Leber optic neuropathy
  • Anticardiolipin antibody (ACA) testing should be performed, and an increased level is considered a risk factor for visual-field defect progression. [11]
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Imaging Studies

Optic nerve head and/or retinal nerve fiber analysis

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 with CT scanning because of its higher sensitivity in ruling out tumors that cause compressive optic neuropathy. [12]

Controversy exists as to whether neuroimaging should be performed routinely. Consider referral to a neurophthalmologist upon doubt.

Neuroimaging should be performed in any patient 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

Carotid Doppler testing

If indicated, carotid Doppler testing is recommended to rule out carotid insufficiency.

Chest radiography

Chest radiography may be considered to rule out sarcoidosis.

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Other Tests

To rule out nocturnal hypotension, 24-hour ambulatory blood pressure monitoring or sleep study may be considered.

The diurnal tension curve may need to be determined. 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 and diagnose the condition as primary open-angle glaucoma.

Multifocal electroretinograms (mfERGs) provides an index of identification for a glaucomatous optic neuropathy in normal-tension glaucoma. [13]

Future diagnostic modalities - Ocular blood flow analysis (see below)

  • Scanning laser ophthalmoscopy - Retinal and choroidal, superficial optic nerve head
  • Doppler ultrasonography - Carotid arteries
  • Confocal scanning laser Doppler flowmetry (Heidelberg Retinal Flowmetry) - Short posterior ciliary artery circulation, optic nerve head
  • Diffuse tension MRI (DTI) - Reduction of the optic radiation volume in patients with normal-tension glaucoma, in relation to arterial hypertension and cerebral microangiopathy stage [14]
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Histologic Findings

Findings include posterior deformation of the cribriform plate, with compression of the lamina due to direct deformation by secondary vascular compression, resulting in glial atrophy.

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