Ophthalmology

*Glaucoma*
The glaucomas are a group of eye disorders characterized by progressive optic nerve damage at least partly due to
increased intraocular pressure (IOP).

 Glaucoma can occur at any age but is 6 times more common among people > 60 yr.

Classification of glaucoma:
1) Open angle.
2) Closed angle.
Note: The “angle” refers to the angle formed by the junction of the iris and cornea at the periphery of the anterior
chamber.

Other classification:
1. Primary (cause of outflow resistance or angle closure is unknown).
2. Secondary (outflow resistance results from another disorder), accounting for > 20 adult types.

The angle is where > 98% of the aqueous humor exits the eye via either the trabecular meshwork and Schlemm's
canal (the major pathway, particularly in the elderly) or the ciliary body face and choroidal vasculature. These outflow
pathways are not simply a mechanical filter and drain but instead involve active physiologic processes.

Developmental Abnormalities of the Anterior Chamber Angle Causing Glaucoma (classification Based on Mechanisms of
Outflow Obstruction):

Means Disorders
High insertion of peripheral iris Axenfeld-Rieger syndrome
Peters' anomaly
Incomplete development of trabecular meshwork or Congenital (infantile) glaucoma
Schlemm's canal Glaucomas associated with other developmental
abnormalities
Fine strands that contract to close angle Aniridia

Pathophysiology:

- Axons of retinal ganglion cells travel through the optic nerve carrying images from the eye to the brain.

- Damage to these axons causes ganglion cell death with resultant optic nerve atrophy and patchy vision loss.

- Elevated IOP (in unaffected eyes, the average range is 11 to 21 mm Hg) plays a role in axonal damage, either by
direct nerve compression or diminution of blood flow.

- IOP is determined by the balance of aqueous secretion and drainage.

- Elevated IOP is caused by inhibited or obstructed outflow, not oversecretion.

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- In open-angle glaucoma, IOP is elevated because outflow is inadequate despite an angle that appears
unobstructed.

- In angle-closure glaucoma, IOP is elevated when a physical distortion of the peripheral iris mechanically blocks
outflow.

Diagnosis:

 Characteristic visual field defects.

 Exclusion of other causes.
 IOP usually > 21 mm Hg (but not required for the diagnosis).

Glaucoma should be suspected in a patient with any of the following:

 Typical visual field defects.

 Abnormal optic nerve on ophthalmoscopy.
 Elevated IOP.

*Closed angle glaucoma*

Angle-closure glaucoma is glaucoma associated with a physically obstructed anterior chamber angle, which may be
chronic or, rarely, acute.

Pathophysiology:

Angle closure may be primary (cause is unknown) or secondary to another condition and can be acute, subacute
(intermittent), or chronic.

Primary angle-closure glaucoma:

- Narrow angles are not present in young people. As people age, the lens of the eye continues to grow. In some but
not all people, this growth pushes the iris forward, narrowing the angle.

- In people with narrow angles, the distance between the pupillary iris and the lens is also very narrow.

- When the iris dilates, forces pull it centripetally and posteriorly causing iris–lens contact, which prevents aqueous
from passing between the lens and iris into the anterior chamber (this mechanism is termed pupillary block).

- Pressure from the continued secretion of aqueous into the posterior chamber by the ciliary body pushes the
peripheral iris anteriorly (a forward-bowing iris called iris bombe), closing the angle.

- This closure blocks aqueous outflow, resulting in rapid (within hours) and severe (> 40 mm Hg) elevation of IOP.

- Because of the rapid onset, this condition is called primary acute angle-closure glaucoma and is an ophthalmic
emergency requiring immediate treatment.

Intermittent angle-closure glaucoma:

- Occurs if the episode of pupillary block resolves spontaneously after several hours, usually after sleeping supine.
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Chronic angle-closure glaucoma:

- Occurs if the narrowing of the angle develops slowly, allowing scarring between the peripheral iris and trabecular
meshwork; IOP elevation is slow.

Pupillary dilation (mydriasis) can push the iris into the angle and precipitate acute angle-closure glaucoma in any person
with narrow angles. This development is of particular concern when applying topical agents to dilate the eye for
examination (Cyclopentolate, Phenylephrine), or for treatment (Homatropine) or when giving systemic drugs that have
the potential to dilate the pupils (Scopolamine).

Secondary angle-closure glaucomas:

- In these patients, the mechanical obstruction of the angle is due to a coexisting condition, such as proliferative
diabetic retinopathy (PDR), ischemic central vein occlusion, uveitis, or epithelial down-growth.

- Contraction of a neovascular membrane (in PDR) or inflammatory scarring associated with uveitis can pull the
iris into the angle.

Symptoms and Signs:

Symptoms of acute angle closure:

1. Severe ocular pain.

2. Severe ocular redness.

3. Decreased vision.

4. Colored halos around lights.

5. Headache.

6. Nausea.

7. Vomiting.

8. Intraocular pressure (IOP) is elevated (40 to 80 mm Hg).

Physical examination:

1. Conjunctival hyperemia.
2. Hazy cornea.
3. Fixed mid-dilated pupil.
4. Anterior chamber inflammation.
5. The optic nerve is difficult to visualize due to corneal edema.

Note: The systemic complaints may be so severe that patients are misdiagnosed as having a neurologic or GI problem.

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Note: Immediate treatment of the acute condition with multiple topical and systemic drugs is required to prevent
permanent vision loss, followed by the definitive treatment, iridotomy.

Chronic angle-closure glaucoma:

- This type of glaucoma manifests similarly to open-angle glaucoma.

1. Some patients have ocular redness.

2. Blurred vision.

3. Headache that lessens with sleep (perhaps due to sleep-induced miosis and posterior displacement of the lens by
gravity).

4. On gonioscopy: the angle is narrow, and peripheral anterior synechiae (PAS).

5. IOP may be normal but is usually higher in the affected eye.

Diagnosis:

 Acute: Measurement of IOP and clinical findings.

 Chronic: Gonioscopy showing peripheral anterior synechiae and characteristic optic nerve and visual field
abnormalities.

Treatment:
Treatment must be initiated immediately, because vision can be lost quickly and permanently. The patient should receive
several drugs at once. A suggested regimen is:

1. Timolol: 0.5% one drop q 30 min for 2 doses.

2. Pilocarpine: 2 to 4% one drop q 15 min for the first 1 to 2 h.
3. Apraclonidine: 0.5 to 1% one drop q 30 min for 2 doses.
4. Acetazolamide: 500 mg po initially followed by 250 mg q 6 h.
5. Surgical treatment: laser peripheral iridotomy (LPI).

* Primary Open-Angle Glaucoma*

Primary open-angle glaucoma is a syndrome of optic nerve damage associated with an open anterior chamber
angle and an elevated or sometimes average intraocular pressure (IOP).

Risk factors:
1. Older age.
2. Family history.
3. Black race.
4. Thinner central corneal thickness.
5. Systemic hypertension.
6. Diabetes.

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7. Myopia.

Pathophysiology:

- IOP can be elevated or within the average range.

 Elevated-pressure glaucoma:

o Elevated IOP > 21 mm Hg.

o Aqueous humor drainage is inadequate, whereas production by the ciliary body is normal.

 Normal- or low-pressure glaucoma:

o IOP is within the average range.

o Optic nerve damage and visual field loss typical of glaucoma are present.

o These patients have a higher incidence of vasospastic diseases (eg, migraines, Raynaud's syndrome).

Symptoms and Signs:

Early symptoms are uncommon. Usually, the patient becomes aware of visual field loss only when optic nerve
atrophy is marked.

1. Missing stairs if their inferior visual field has been lost, noticing portions of words missing when reading, or
having difficulty with driving.

2. Findings on examination include:

- An unobstructed open angle on gonioscopy and characteristic optic nerve appearance and visual field
defects.

- IOP may be normal or high but is almost always higher in the eye with more optic nerve damage.

3. Optic nerve changes.

4. Visual filed defect.

Optic nerve appearance:

- The optic nerve head (disk) is normally a slightly vertically elongated circle with a centrally located depression
called the cup.
- The neurosensory rim is the tissue between the margin of the cup and the edge of the disk and is composed of the
ganglion cell axons from the retina.

Characteristic optic nerve changes include:

1. Increased cup:disk ratio.

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2. Thinning of the neurosensory rim.

3. Pitting or notching of the rim.
4. Nerve fiber layer hemorrhage that crosses the disk margin (ie, Drance hemorrhage or splinter hemorrhages).
5. Vertical elongation of the cup.
6. Quick angulations in the course of the exiting blood vessels.

Note: Thinning of the neurosensory rim over time can be solely diagnostic of glaucoma regardless of the IOP or
visual field. However, most initial diagnoses of glaucoma involve some visual field change.

Visual field defects:

- Visual field changes caused by lesions of the optic nerve.

 Nasal step defects (which do not cross the horizontal meridian).

 Arcuate (arc-shaped) scotomata extending nasally from the blind spot.
 Temporal wedge defects.
 Paracentral scotomata.

Diagnosis:

 Visual field testing.

 Ophthalmoscopy.
 Measurement of IOP.
 Exclusion of other optic neuropathies.

Treatment:

 Decreasing IOP 20 to 40%.

 Initially, drugs (eg, prostaglandin analogs, β-blockers such as timolol.
 Sugary: Laser trabeculoplasty.