Glaucoma

I. What every physician needs to know.

Glaucomas are a group of eye disorders characterized by progressive optic nerve damage at least partly due to increased intraocular pressure (IOP). This causes the characteristic visual field defect associated with progressive loss of visual acuity. When classified simply, it is primarily of 2 types:

Open angle glaucoma – addressed in this chapter
Narrow angle/angle closure glaucoma

II. Diagnostic Confirmation: Are you sure your patient has open angle glaucoma?

Clinical suspicion – based on typical signs/symptoms
Diagnostic confirmation – by ophthalmoscopy, gonioscopy, visual field examination, and measurement of IOP

A. History Part I: Pattern Recognition:

Early diagnosis is difficult. The typically asymmetric deficits contribute to delay in recognition. However, some patients have complaints such as missing stairs if their inferior visual field has been lost, noticing portions of words missing when reading or having difficulty with driving. Usually, the patient becomes aware of visual field loss only when optic nerve atrophy is marked.

Open/unobstructed angle on gonioscopy
Characteristic optic nerve changes
Visual field defects

B. History Part 2: Prevalence:

Glaucoma is a leading cause of irreversible blindness, second only to macular degeneration. Glaucoma can occur at any age but is 6 times more common among people over 60 years. Prevalence of primary open angle glaucoma (POAG) is 3-4 times higher in blacks than in Caucasians; in addition, blacks are up to 6 times more susceptible to optic disc nerve damage than Caucasians.

In a white population at risk for glaucoma, visual field loss can be expected to develop in about 3% of subjects over 10 years of follow-up without treatment. Risk increases with age and IOP. Patients over 40 years and those who have risk factors for open-angle or angle-closure glaucoma should receive a comprehensive eye examination every 1 to 2 years.

Pathophysiology

IOP can be elevated or within the average range.

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 21mm Hg) plays a role in axonal damage, either by direct nerve compression or diminution of blood flow. However, the relationship between pressure and nerve damage is variable.

Of people with IOP over 21mm Hg (i.e., ocular hypertension), only about 1 to 2% per year (about 10% over 5 years) develop glaucoma. Additionally, about one third of patients with glaucoma do not have IOPs over 21mm Hg (known as low-tension glaucoma or normal-tension glaucoma).

IOP is determined by the balance of aqueous secretion and drainage. Elevated IOP is caused by inhibited or obstructed outflow, not oversecretion. 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.

C. History Part 3: Competing diagnoses that can mimic open angle glaucoma.

Personal or family history of glaucoma. Past ocular history includes the following:

History of eye pain or redness or multicolored halos

Headache

Previous ocular disease

Previous ocular surgery

Ocular/head trauma

Past medical history

Current medications

Other optic neuropathies

D. Physical Examination Findings.

The defining characteristic is optic nerve damage as evidenced by an abnormal optic disk. Glaucoma should be suspected in a patient with any of the following:

Typical visual field defects
Abnormal optic nerve on ophthalmoscopy
Elevated or normal IOP

E. What diagnostic tests should be performed?

Visual field testing
Ophthalmoscopy
Measurement of IOP
Exclusion of other optic neuropathies

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Patients suspected of having open angle glaucoma may need work-up to rule out other causes for optic neuropathy, including, but not limited to, complete blood count, erythrocyte sedimentation rate (ESR), serology for syphilis and if suggested by the pattern of visual field loss, neuroimaging.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Neuroimaging
Fundus photography provides a permanent record of the appearance of the optic disc also useful for future references.

III. Default Management.

Three methods are available: The type of glaucoma determines the appropriate method:

Drugs
Laser surgery
Incisional surgery

A. Immediate management.

Treatment goals

Vision lost by glaucoma cannot be recovered because the axonal damage caused by the prolonged elevated IOP is irreversible. Decreasing IOP 20-40% to prevent further optic nerve and visual field damage is the primary goal. All patients should get a formal ophthalmology consultation prior to initiation of treatment

Initially treatment of choice (drugs)

prostaglandin analogs
β-blockers such as timolol
α₂-selective adrenergic agonists
cholinergic agonists
carbonic anhydrase inhibitors

B. Physical Examination Tips to Guide Management.

Initial treatment is usually drug therapy, proceeding to laser therapy and then incisional surgery if the target IOP is not met. Surgery may be the initial treatment of choice if IOP is extremely high. Surgical options include:

Laser trabeculoplasty

A guarded filtration procedure

Possibly tube shunts

Cyclodestructive procedures

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

No consensus exists on what the appropriate medical treatment is for preventing or delaying the damage due to POAG when a patient has only elevated IOP and no other signs of POAG. To date, no one has been able to define conclusively which subgroups will develop damage if left untreated.

Typically, to gauge effectiveness, clinicians start drugs in only one eye (one-eye trial), once improvement in the treated eye has been confirmed at a subsequent visit (typically 1 to 4 weeks later), both eyes are treated. This is mailny useful in helping to decide whether or not to treat (i.e., if the medication is effective in achieving good pressure reduction without adverse effects).

D. Long-term management.

Refer to ophthalmologist for further evaluation, management and follow-up.

Neuro-ophthalmology consultation may have a role in those patients who are experiencing progressive visual loss that does not appear to follow a typical glaucomatous pattern or if there are systemic symptoms or complaints.

Depending on the amount of optic nerve damage and level of IOP control, POAG patients may need to be seen from every 2 months to yearly, even sooner if a marked lack of IOP control is present

E. Common Pitfalls and Side-Effects of Management

Indications of treatment

Patient factors
Poor reliability on visual field examination or patient whose optic nerve is difficult to visualize
History of vascular occlusion
Signs of damage consistent with glaucomatous optic neuropathy are observed
Progressive cupping, even in the absence of visual field loss
If pressures are consistently above 28-30mm Hg

Medication

Beta-blockers: adverse effects are due to systemic absorption of the drug :decreased cardiac output, and bronchoconstriction (bronchospasm), bradycardia, heart block, hypotension, depression or anxiety, and sexual dysfunction may be initiated or exacerbated. Ocular adverse effects may include blurred vision, eye ache, and corneal anesthesia.
Alpha2-adrenergic agonists: systemic adverse effects include dry mouth, fatigue, and drowsiness. Ocular adverse effects include allergic (follicular) conjunctivitis and contact dermatitis.
Carbonic anhydrase inhibitors: adverse effects are relatively rare but include superficial punctate keratitis, acidosis, paresthesias, anorexia, nausea, depression, dysgeusia, and lassitude
Prostaglandin analogs: adverse effects include conjunctival hyperemia, iris pigmentation, CME, and uveitis.

Management regimens

Beta-blockers

Timolol maleate/hemihydrate (Timoptic 0.25%, 0.5%; Timoptic XE, Betimol 0.25%, Istalol) – non-selective.
Levobunolol 0.25%, 0.5%, (Betagan) – non-selective
Carteolol ophthalmic (Cartrol, Ocupress) – blocks beta1 and beta2-receptors, and has mild intrinsic sympathomimetic activity (ISA), with possibly fewer cardiac and lipid profile adverse effects.
Betaxolol ophthalmic (Betoptic-S) – beta1-selective adrenergic antagonist, with possibly less pulmonary effects than non-selective agents. IOP-lowering effect is slightly less than non-selective beta-blockers.
Metipranolol hydrochloride (OptiPranolol) – beta-adrenergic blocker that has little or no intrinsic sympathomimetic effects and membrane stabilizing activity. Has little local anesthetic activity.
Levobetaxolol (Betaxon) – selectively blocks beta1-adrenergic receptors.

Alpha2-adrenergic agonists

Apraclonidine 0.5%, 1% (Iopidine) – selective alpha-adrenergic agonist without significant local anesthetic activity. Has minimal cardiovascular effect.
Brimonidine (Alphagan-P 0.2%, 0.15%, 0.1%)

Carbonic Anhydrase inhibitors (topical)

Dorzolamide (Trusopt) – more commonly used concomitantly with other topical medicines.
Brinzolamide (Azopt) – may cause less ocular discomfort on instillation, secondary to a buffered pH, but can still cause foreign body sensation.
Acetazolamide (Diamox) – used for adjunctive treatment of chronic simple (open-angle) glaucoma and secondary glaucoma and preoperatively in acute angle-closure glaucoma when delay of surgery desired to lower IOP.
Methazolamide (Neptazane)

Various combinations of above drugs are also available.

Prostaglandin analogs

Latanoprost 0.005% (Xalatan), Bimatoprost (Lumigan), Travoprost ophthamic solution (Travatan), Unoprostone (Rescula).

IV. Management with Co-Morbidities

N/A

H. Primary Lung Disease (COPD, Asthma, ILD)

Careful monitoring needed in patients on beta-blockers.

V. Transitions of Care

D. Arranging for Clinic Follow-up

Ophthalmology referral and follow-up.

2. What tests should be conducted prior to discharge to enable best clinic first visit.

None

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.