Glaucoma Disease

BASICS

DESCRIPTION

Primary angle-closure glaucoma results from obstruction of aqueous humor outflow through the trabecular meshwork by peripheral iris apposition to the cornea which causes a consequent elevation in intraocular pressure (IOP). The underlying mechanism is pupillary block, in which aqueous egress through the pupil is limited causing forward iris displacement. Angle-closure glaucoma can occur in subacute, acute, and chronic forms and is associated with an anatomically narrow anterior chamber angle; the angle comprises the peripheral iris, anterior ciliary body, trabecular meshwork, and peripheral cornea and can only be observed with a special examination technique called gonioscopy. In its acute form, primary angle-closure glaucoma is an ophthalmic emergency with a natural history of severe visual loss.

System(s) affected: Nervous
Genetics: Polygenic inheritance; first degree relatives have a 2-5% lifetime risk
Incidence/Prevalence in USA:
- 100 cases/100,000 population
- 500/100,000 (Blacks and Asians more common than Caucasians)
Predominant age: 55-70
Predominant sex: Female > Male

SIGNS AND SYMPTOMS

Subacute
- Dull ache in or around one eye
- Mildly blurred vision
- Symptoms occur when watching TV or movies in dark room, reading, or when fatigued. Relieved by sleep or rest.
- Normal intraocular pressure (10-23 mmHg)
- Shallow anterior chamber
- Iris bombé
- Intermittent peripheral anterior synechiae
- Enlarged pupil
Acute
- Ocular pain
- Blurred vision
- Lacrimation
- Halos around lights
- Frontal headache
- Nausea and vomiting
- Symptoms likely to occur with times of emotional stress and with activities as for subacute form
- Elevated intraocular pressure (usually 40-80 mm Hg)
- Corneal microcystic edema
- Lid edema, conjunctival hyperemia, and circumcorneal injection
- Fixed mid-dilated pupil, often oval
- Shallow anterior chamber often with inflammatory reaction
Chronic
- May have symptoms of subacute form or may be asymptomatic
- Multiple peripheral anterior synechiae
- Normal or elevated intraocular pressure
- Increased cup to disc ratio
- Normal pupil

CAUSES

Predisposing ocular anatomy

RISK FACTORS

Small cornea
Hyperopia
Shallow anterior chamber
Eskimo ancestry
Female sex
Use of antidepressants or other drugs with cholinergic inhibition
Cataract
Iris and ciliary body cysts

DIAGNOSIS

LABORATORY

None

Drugs that may alter lab results: N/A
Disorders that may alter lab results: N/A

PATHOLOGICAL FINDINGS

Corneal stromal and epithelial edema
Endothelial cell loss
Iris stromal necrosis
Anterior subcapsular cataract (glaukomflecken)
Optic disc congestion, cupping
Optic nerve atrophy

SPECIAL TESTS

Gonioscopy

IMAGING

N/A

DIAGNOSTIC PROCEDURES

Careful ophthalmic examination including indentation gonioscopy and tonometry

TREATMENT

APPROPRIATE HEALTH CARE

Acute form: inpatient admission from office or emergency room
Other forms: outpatient management
Ophthalmology consultation

GENERAL MEASURES

For acute form:
- Establish intravenous access for administering medications; antiemetics may be necessary
- Definitive treatment: laser iridotomy once the attack is broken, intraocular pressure is normalized, and intraocular inflammation has subsided

SURGICAL MEASURES

Surgical/laser interventions:
- Peripheral iridectomy
- Argon or Nd:YAG laser iridotomy (procedure of choice for subacute and chronic forms)
- Argon laser gonioplasty

ACTIVITY

For acute form - bedrest until attack subsides

DIET

Usual for patient

PATIENT EDUCATION

Usually patients need bilateral treatment since second eye is at risk for same disease process
For patient education materials favorably reviewed on this topic, contact:
- Foundation for Glaucoma Research, 490 Post Street, Suite 830, San Francisco, CA 94102, (415)986-3162
- American Academy of Ophthalmology, 655 Beach Street, San Francisco, CA 94109, (415)561-8500

FOLLOW UP

PREVENTION/AVOIDANCE

Prophylactic laser treatment of second eye

POSSIBLE COMPLICATIONS

Chronic corneal edema
Corneal fibrosis and vascularization
Iris atrophy
Cataract
Lens subluxation
Optic atrophy
Malignant glaucoma
Central retinal vein occlusion

EXPECTED COURSE AND PROGNOSIS

Varies with delay of patient presentation and severity of attack
Preceding chronic angle-closure may have caused optic atrophy
Recurrence is quite rare following peripheral iridotomy or iridectomy and implies a rare variant known as the iris plateau syndrome

MISCELLANEOUS

ASSOCIATED CONDITIONS

Cataract
Microphthalmos
Hyperopia

AGE-RELATED FACTORS

Pediatric: Rare
Geriatric: Secondary angle closure glaucoma can be caused by many common eye conditions in the elderly including cataract, ocular surgery and diabetes
Others: N/A

PREGNANCY

N/A

OTHER NOTES

Medications (higher risk) that may exacerbate angle-closure glaucoma:
- Systemic or topical anticholinergics
- Topical sympathomimetics
- Antihistamines
- Phenothiazines
- Antidepressants
Medications (lower risk) that may exacerbate angle-closure glaucoma:
- Benzodiazepine
- Carbonic anhydrase inhibitors
- CNS stimulants (including cocaine)
- MAO inhibitors
- Systemic sympathomimetics
- Theophylline
- Vasodilators

ABBREVIATIONS

NAG = narrow angle glaucoma

Clinical Investigations

ROLE OF HOMOEOPATHY

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