Glaucoma
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[edit] Glaucoma
G. Robert Lesser
Deborah A. Darnley-Fisch
Talya H. Kupin
Rhett M. Schiffman
Glaucoma is a term used for a group of diseases characterized by damage to the optic nerve and visual field loss, usually associated with an elevated intraocular pressure (IOP). The optic nerve becomes pale and cupped, and other abnormalities may be noted as well (Fig. 173-1). Once the optic nerve has been damaged, the visual loss is irreversible. For this reason early detection and prompt treatment are essential.
[edit] EPIDEMIOLOGY
Glaucoma is one of the leading causes of blindness in the United States, affecting at least 2 million people, and is the leading cause of blindness among African-Americans. The Baltimore Eye Survey revealed that more than half of these individuals are unaware that they have the disease.[1] Another 5 million to 10 million are at risk of developing the disease over their lifetime. The medical and financial implications of the disease and its treatment are staggering, and delayed diagnosis is a major component of glaucoma-induced blindness.
[edit] PATHOPHYSIOLOGY
Damage to the axons of the retinal ganglion cells as they course through the optic nerve results in cell death and characteristic optic atrophy. The pattern of the atrophy is determined by the anatomy of the optic nerve, but it is not clear whether the damage is due to mechanical compression of the axons from elevated IOP or due to indirect damage from vascular compromise. Most intervention has been directed toward lowering IOP, as well as modifying blood flow to the optic nerve. An exciting new development is the use of neuroprotective agents to protect the retinal ganglion cell axons from damage.
[edit] KEY RISK FACTOR: INTRAOCULAR PRESSURE ELEVATION
The key risk factor for losing vision is elevated IOP. The normal range of IOP is 11 to 21 mm Hg, with a mean of 15.5 mm Hg. The normal pressure curve in the general population is not a normal gaussian distribution, but is skewed toward the higher pressures (Fig. 173-2).
Almost 80% of patients with glaucoma eventually have a documented elevation of IOP. Although a direct prospective study of treated vs. untreated glaucoma patients has not been formally conducted, there appears to be a direct correlation between the magnitude and duration of IOP elevation and subsequent visual loss.
Up to 20% of patients with typical optic nerve and field changes have IOP measurements completely in the normal range. In these patients other unknown factors such as vasospasm, hemodynamic perturbations, or structural abnormalities appear to contribute to the optic nerve damage.
Approximately 5 million to 10 million Americans have elevated IOP without optic nerve or visual field damage, a condition called ocular hypertension. It is not known how many of these people with ocular hypertension progress to actual glaucoma, but current estimates are approximately 1% per year. The rate of conversion of ocular hypertension to glaucoma, as well as the benefit of prophylactic treatment to lower IOP, is being studied in a 10-year prospective trial by the National Institutes of Health (NIH).
Many factors influence the IOP. It varies throughout the day and is often higher early in the morning. This pressure fluctuation is subject to the individual's diurnal rhythm and may vary greatly between patients. The IOP increases slightly when the patient is supine but may be lowered during sleep. Mean IOP increases with age and is higher in African-Americans.
Although IOP rises only slightly with increased systemic hypertension, it may be lowered by medications administered systemically to lower blood pressure, such as β-blockers and calcium channel blockers. There are conflicting reports with respect to the effect of caffeine, smoking, and exercise on IOP. There is also a small group of people who are steroid responders. In these individuals there can be a large elevation of IOP in response to systemic steroids, topical ocular steroids, and in rare instances the use of topical dermatologic steroid preparations close to the eyes.
This marked variability makes an isolated measurement of IOP a poor indicator for predicting the risk of glaucoma, and seriously limits any diagnosis that relies on IOP alone. When 10,444 individuals in East Baltimore were examined, 194 cases of open-angle glaucoma were found, but 59% of those individuals eventually diagnosed with the disease actually had normal pressures during screening.[1]
[edit] OTHER RISK FACTORS
There is now evidence of a genetic component to many of the glaucomas, and glaucoma should be suspected in all patients with a positive family history, especially after age 40. The disease is also more common in patients with diabetes, high myopia, systemic hypertension, cardiovascular disease, and possibly vasospasm (Box 173-1). The risk of optic nerve damage increases with age. African-Americans are at particularly high risk because they tend to develop visual loss at an earlier age (in their thirties), and their disease can be very aggressive. It has been estimated that one in 10 elderly African-Americans has glaucoma, a rate five times higher than elderly white patients.
| Box 173-1 - Risk Factors for Glaucoma |
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[edit] PATIENT EVALUATION
[edit] General
Patients with early and moderate primary open-angle glaucoma are asymptomatic. Only when there is advanced optic nerve damage may they notice dimmed or blurred vision. Rarely can they detect peripheral vision loss, and usually monocular patching is necessary for patients to be aware of their visual defect. Conjunctival injection, ocular pain, or halo vision may be noted by patients with intermittent angle-closure glaucoma. In addition to these symptoms, nausea and vomiting can be dramatic during acute angle-closure attacks.
Because symptoms may be lacking, subtle, or generalized, it is important to obtain a careful ocular and general medical history. Ocular history may reveal recent or remote ocular trauma or intraocular surgery. Previous ocular inflammatory diseases such as herpes zoster ophthalmicus or uveitis also indicate patients at higher risk for glaucoma. The general medical history may reveal associated systemic diseases such as diabetes, hypertension, herpes zoster, sarcoidosis, and ankylosing spondylitis.
A review of patient medications is vital, since steroids may cause a marked elevation of IOP in susceptible individuals. Anticholinergics, such as atropine, tropicamide, and scopolamine, may precipitate acute angle-closure glaucoma. Other relatively common medications have some anticholinergic effects as well, including antihistamines, antipsychotics, and antiparkinsonian medications (Box 173-2).
| Box 173-2 - Drugs That May Precipitate Angle-closure Glaucoma |
Modified from Mandelkorn RM, Zimmerman TJ. In Ritch R, Shields MB, editors: The secondary glaucomas, St Louis, 1982, Mosby.
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Finally, a family history of glaucoma should be sought from every patient in whom the disease is suspected. The risk for glaucoma is at least 10 times higher in individuals with a first-degree relative with the disease.
[edit] IOP Determination
IOP is measured by determining the force needed to indent the eye. The most common device available to the general practitioner for measurement of IOP has been the Schiøtz tonometer (Fig. 173-3). With the patient in the supine position, a metal footplate plunger is gently placed on the anesthetized cornea and the IOP is determined by the displacement of a weighted plunger that protrudes through the footplate. The advantage of this technique is the durability and portability of the device. It is, however, sometimes difficult to apply and may be uncomfortable for the patient. Moreover, it underestimates IOP in highly myopic patients due to decreased scleral rigidity.
Optometrists may use a noncontact air puff tonometer in which the eye is indented with a rapid impulse of air. This technique has the advantage of not requiring topical anesthetic drops and minimizes the chance of cross-contamination between patients, since only the stream of air actually touches the cornea. It is somewhat uncomfortable for patients, requires moderately expensive equipment, and tends to give measurements higher than actual. Many public health screenings are conducted with this device, and the results should not be used to establish a diagnosis or follow a patient.
Ophthalmologists usually use Goldmann's applanation tonometry, in which a small plastic device mounted on a slit lamp indents the cornea, and the pressure is determined by displacement of the tear film. This requires a topical anesthetic and is very accurate and reproducible. The technique requires special equipment and training.
A newer device for measuring IOP is the Tonopen (Fig. 173-4), a handheld device in which a 1.02-mm central plunger is connected to a microprocessor that measures the applied force. This device and its successors offer the general practitioner a convenient way of screening for elevated IOP. The device is portable and battery operated, and pressures may be taken with the patient in any position. After instillation of a topical anesthetic, proparacaine HCl (Alcaine), the tip of the Tonopen is gently applied to the central cornea until an audible tone is heard, and the pressure measurement is immediately available on a small display within the handle. A disposable sterile cap is used on the tip of the Tonopen. Although significantly more expensive than a Schiøtz tonometer, the Tonopen is easy to use with limited training and much more comfortable for both the patient and physician. The Tonopen tends to overread pressures below 5 mm Hg and underread pressures over 30 mm Hg, but for screening purposes these limitations are not significant.
[edit] Visual Fields
Measurement of peripheral vision loss requires specialized equipment. Ophthalmologists often use automated perimeters with standardized parameters. Examples of common patterns of visual field loss with glaucoma are shown in Fig. 173-5.
[edit] Optic Disc Abnormalities
The optic nerve can usually be visualized with a direct ophthalmoscope, even through an undilated pupil, and is thus accessible to the general practitioner. Findings suggestive of glaucoma include a large cup/disc (c/d) ratio (only 6% of the normal population has a c/d ratio greater than 0.50), narrowed optic disc neural rim, asymmetric cupping between the two eyes, vertical elongation of the cup, focal notching, disc pallor, and superficial disc hemorrhages (see Fig. 173-1).
[edit] GLAUCOMA SCREENING
The general practitioner needs to screen for glaucoma during routine physical examinations if risk factors are present (see Box 173-1). If the IOP is elevated or the optic nerve appears abnormal (see Fig. 173-1), a patient should be referred for formal ophthalmologic testing. If either factor cannot be assessed adequately or if the patient has additional risk factors, the patient should also be referred. A recently developed device called a frequency doubled perimeter (FDP) has been shown in several studies to allow for rapid (2 to 3 minutes) assessment of moderate to severe visual field loss and may prove useful as a screening device in a primary care setting.
[edit] DIFFERENTIAL DIAGNOSIS
The general practitioner may encounter patients with glaucoma in two clinical settings. The first is a patient with a white, quiet eye, in whom the disease is suspected because of risk factors, elevated IOP found during screening examination, optic disc cupping and pallor found during routine funduscopic examination, or painless visual loss. Commonly encountered glaucomas in this setting are shown in Box 173-3. In the second setting the patient presents with an inflamed red eye, and an elevated IOP is found during the evaluation (Box 173-4). The treatment varies according to which setting is encountered.
| Box 173-3 - Elevated IOP and the White Eye |
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| Box 173-4 - Elevated IOP and the Red Eye |
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[edit] Primary Open-angle Glaucoma
Primary (chronic) open-angle glaucoma is the most common form of glaucoma. Patients initially have no symptoms until the disease is far advanced, at which time they have sustained significant field loss close to fixation. There is blockage of aqueous outflow in the trabecular meshwork. The pressure is usually elevated above 21 mm Hg and is often over 30 mm Hg. There is considerable variation in the amount of damage to the optic nerve for a given pressure. This is also true for normal tension glaucoma, in which the IOP is consistently in the normal range but the patients sustain optic nerve and visual field change identical to that seen with primary open-angle glaucoma.
Treatment consists of a stepwise progression of drops, pills, laser surgery, and filtration surgery, modified to take into account the overall health of an individual and side effects from the medications (Box 173-5).
| Box 173-5 - Therapy for Primary Open-angle Glaucoma |
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[edit] Acute Angle-closure Glaucoma
Angle-closure glaucoma usually occurs in hyperopic individuals, those with thick convex glasses that magnify images. Acute angle-closure glaucoma occurs when the pupillary margin of the iris is pushed against the surface of the lens, a configuration called pupillary block. Aqueous fluid can no longer flow forward through the pupil, resulting in an increase in the pressure behind the iris. The iris is then pushed forward, blocking the trabecular meshwork. This results in a raised IOP. As the IOP increases, the lens is then pushed further forward, increasing the pupillary block, resulting in an upward spiral of increasing IOP over several hours.
Pupillary block is often precipitated in predisposed individuals by pupillary dilation. This can occur several hours after patients have been pharmacologically dilated for examination, when pupils dilate in the dark, or as a result of dilation from medications with anticholinergic effects such as antihistamines and some cold remedies (see Box 173-2). This sudden rise in IOP often results in severe ocular pain and can be accompanied by referred gastrointestinal pain with nausea and vomiting. The vision is often very blurred, and patients may complain of halos around lights.
When examined with a handlight, the cornea appears cloudy or steamy from corneal edema and the anterior chamber is often very shallow. The pupil is commonly mid-dilated, fixed, and can be slightly eccentric. The sclera is injected and there can be profuse reflex tearing. The eye may feel firm to touch, and the IOP is very elevated; pressures of greater than 50 mm Hg are often seen. The fundus is difficult to see through the cloudy cornea. Examination of the opposite eye should demonstrate shallowing of the anterior chamber as well (Fig. 173-6).
If left untreated, acute angle-closure glaucoma can lead to permanent blindness. The optic nerve may be severely damaged and a secondary retinal vascular occlusion can occur. Damage to the corneal endothelium may result in thickening and clouding of the cornea (bullous keratopathy), and cataract formation is accelerated.
When the patient is first seen, the immediate goal is to reduce the IOP. Corneal indentation with an anesthetic (proparacaine)-soaked cotton applicator may help break the pupillary block. Medications to acutely lower IOP are shown in Box 173-6. Definitive treatment for angle-closure glaucoma is an iridectomy to bypass the mechanical blockage of the iris. This usually can be achieved with a YAG or argon laser, although occasionally a surgical iridectomy is necessary. Following an acute attack a patient may have persistently elevated pressures despite adequate iridectomies as a result of damage to the trabecular meshwork and may require chronic medication or surgery.
| Box 173-6 - Medical Therapy for Angle-closure Glaucoma |
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[edit] Neovascular Glaucoma
Patients with extensive ischemia to the retina from diabetic retinopathy or following a central retinal vein occlusion are at risk for developing neovascular glaucoma, a particularly devastating disease that often results in blindness and is difficult to treat. The ischemic retina releases an unidentified angiogenic factor(s), which causes proliferation of new vessels in the retina and on the surface of the iris (rubeosis iridis). These vessels eventually grow across the trabecular meshwork, resulting in mechanical closure of the angle and elevation of the IOP.
The eye may initially be white and quiet, but eventually it becomes inflamed with bulbar injection, corneal edema, and elevated IOP. Fine vessels are invariably present on the surface of the iris but may be difficult to see with a handlight. Occasionally the fibrovascular membrane on the surface of the iris contracts, pulling the darker posterior layer of the iris through the pupil, which is easily visible as ectropion uveae.
Treatment is directed toward reducing IOP and inflammation and removing the underlying stimulus to neovascularization with retinal laser photocoagulation (Box 173-7). In addition to the poor visual prognosis, patients with this diagnosis have a higher incidence of death than age-matched controls, often from cerebral vascular and cardiac causes within 6 to 12 months from the time of diagnosis.
| Box 173-7 - Treatment for Neovascular Glaucoma✢ |
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[edit] Herpes Zoster Ophthalmicus
Herpes zoster affecting the first division of the trigeminal nerve has a high incidence of ocular involvement and is frequently found when there are lesions on the tip of the nose (Hutchinson's sign). Secondary glaucoma often occurs with ocular involvement. The pressure elevation may be asymptomatic. Therefore IOP should be checked in every patient during the acute phase of the disease and probably rechecked 1 to 2 weeks later. The mechanism of the glaucoma is probably direct inflammation of the trabecular mesh work, and the treatment includes systemic acyclovir or Famvir, topical steroids, and antiglaucomatous medications (Box 173-8).
| Box 173-8 - Treatment for Glaucoma in Association With Herpes Zoster |
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[edit] Acute Trauma
Blunt and penetrating trauma to the eye may cause elevated IOP and glaucoma acutely by several different mechanisms. Bleeding directly into the orbit can cause acute proptosis and a very high IOP. The fundus should be visualized immediately to rule out spontaneous arterial pulsations (best seen on the optic nerve), which indicates impending vascular occlusion from the high IOP. The orbit needs to be decompressed immediately, usually with a lateral canthotomy or a controlled fracture of the orbital floor into the maxillary sinus.
Intraocular bleeding may also cause an acute elevation of IOP. Blood and inflammatory debris can plug the trabecular meshwork, and a large clot in the anterior chamber (hyphema) can result in pupillary block glaucoma. The pressure is usually controlled with aqueous suppression (β-blockers and/or carbonic anhydrase inhibitors) and if necessary osmotic agents (Osmoglyn, mannitol). If the pressure is persistently elevated, the anterior chamber can be washed out in the operating room. Patients with sickle cell trait or disease are at increased risk from these anterior segment bleeds, and early surgical intervention is often recommended.
After the acute episode, patients with ocular trauma are at long-term risk for secondary glaucoma. The trabecular meshwork may be permanently damaged, and a laceration into the ciliary body (angle recession) is associated with an elevated IOP. These patients are often completely asymptomatic with white, quiet eyes, and as in chronic open-angle glaucoma, may not be aware of their visual loss until it is far advanced.
[edit] MANAGEMENT OF ELEVATED IOP
Although there are many different types of glaucoma, there are only a limited number of modalities currently available to lower IOP. They are used in a stepwise progression, analogous to the treatment of systemic hypertension.
[edit] Pharmacologic Agents
In the United States, the initial treatment for glaucoma is usually the use of drops to lower the IOP. These drops work by decreasing aqueous production and/or increasing aqueous outflow, and they may be used in combination. When these drops are applied to the eye, a significant portion flow through the nasolacrimal duct, where they are absorbed through the mucous membranes into the systemic circulation. The clinician therefore needs to be aware of the potential side effects of these medications (Table 173-1). The most commonly prescribed antiglaucomatous medications used are β-blockers, which may have adverse cardiovascular and bronchopulmonary effects, such as worsening chronic obstructive pulmonary disease (COPD) and congestive heart failure, precipitation of asthmatic attacks, and increasing sinus bradycardia or heart block. These medications may also raise serum triglycerides and lower high-density lipoprotein (HDL) cholesterol, which may have serious cardiovascular implications, since these medications could be taken for decades. Less obvious effects include impotence in men and confusion in elderly patients.
Table 173-1 Medication Actions and Side Effects
| Medication | Strength | Frequency | Action | Side effects |
|---|---|---|---|---|
| β-Blockers | Reduces aqueous secretion | Local allergy and irritation, bradycardia, heart block, bronchospasm, decreased libido, depression | ||
| Timolol (Timoptic) | 0.25%-0.5% | qd-bid | ||
| Levobunolol (Betagan) | 0.25%-0.5% | |||
| Carteolol (Ocupress) | 1% | |||
| Metipranolol (Optipranolol) | 0.3% | |||
| Betaxolol (Betoptic) | 0.25%-0.5% | |||
| Sympathomimetics | Improves aqueous outflow | Ocular irritation and allergy, adrenochrome deposits, rebound hyperemia, mydriasis, cystoid macular edema in aphakia, hypertension, extrasystoles, headache | ||
| Epinephrine (Glaucon) | 1%-2% | bid | ||
| Dipivefrin (Propine) | 0.1% | bid | ||
| α-Adrenergic agonist | Reduces aqueous secretion | Ocular irritation and allergy, upper lid elevation, mydriasis, bradycardia, dry mouth | ||
| Apraclonidine (Iopidine) | 0.5% | tid | ||
| Direct-and indirect-acting parasympathomimetics | ||||
| Pilocarpine (Isopto Carpine) | 0.5%-6% | qid | Improves aqueous outflow | Miosis, decreased night vision, variable induced myopia, brow ache, exacerbation of cataract, induced-angle closure, retinal tear or detachment |
| Carbachol (Isoptocarbachol) | 0.75%-3% | tid | Improves aqueous outflow | Intense miosis, iris pigment epithelial cysts, induced myopia, cataract, retinal detachment, paradoxic angle closure, punctal stenosis, intense bleeding and inflammation with ocular surgery, abdominal cramps, diarrhea, enuresis, prolonged recovery from succinylcholine |
| Echothiophate iodide (Phospholine Iodide) | 0.03%-0.25% | bid | ||
| Carbonic anhydrase inhibitors | Reduces aqueous secretion | Paresthesias, malaise, lethargy, abdominal cramps, diarrhea, nausea, renal stones, loss of libido, anorexia, depression, hypokalemia, acidosis, aplastic anemia, thrombocytopenia | ||
| Acetazolamide (Diamox) | 125-250 mg | qid | ||
| Acetazolamide (Diamox Sequels) | 500 mg | bid | ||
| Methazolamide (Neptazane) | 25-50 mg | bid-tid | ||
| Hyperosmotic agents | Reduces vitreous volume | Congestive heart failure, headache, subdural and subarachnoid hemorrhages, diabetic ketoacidosis (glycerol) | ||
| Mannitol | 1-2 gm/kg | IV or PO q8-12h | ||
| Isosorbide (Ismotic) | 1.5 gm/kg | |||
| Glycerin (Omoglyn) | 2-3 ml/kg | |||
| Prostaglandin agonist | ||||
| Latanoprost (Xalatan) | 0.003% | QHS | Increased uveoscleral outflow | Conjunctival hyperemia, increased iris and eyelid skin pigmentation, hypertrichosis, ocular irritation and allergy |
| α-Adrenergic agonist | ||||
| Brimonidine tartate (Alphagan) | 0.2% | bid-tid | Reduces aqueous secretion; increased uveoscleral outflow | Conjunctival hyperemia, increased iris and eyelid skin pigmentation, hypertrichosis, ocular irritation and allergy, drowsiness, fatigue |
| Topical carbonic anhydrase inhibitor | ||||
| Dorzolamide hydrochloride (Trusopt) (Azopt) Dorzolamide hydrochloride and timolol in combination (Cosopt) | 2.0% | bid-tid | Reduces aqueous secretion | Ocular irritation and allergy, superficial punctate keratitis, blurred vision and photophobia, same systemic reactions as oral CAI's possible but much less frequent |
Newer topical medications include a prostaglandin analog, two different α-agonists that are clonidine derivatives, and two topical carbonic anhydrase inhibitors. Fatigue, local allergy, and dry mouth are their most common side effects.
When drops fail to adequately lower IOP, carbonic anhydrase inhibitors may be added, such as acetazolamide (Diamox) and methazolamide (Neptazane). They decrease aqueous production in the ciliary body and commonly cause side effects such as generalized fatigue, loss of appetite, and paresthesias in the hands and feet. They may also be associated with renal stones and aplastic anemia and should not be used for patients with a sensitivity or allergy to sulfonamides. Of particular interest to the general practitioner is a transient hypokalemia, which can be severe and may require adjustment of a concurrent diuretic or other antihypertensive medications, as well as potassium replacement.
[edit] Lasers
When the IOP is not controlled with medications, argon laser trabeculoplasty may be used to lower pressure. The procedure is done in an outpatient setting and consists of using a mirrored contact lens to place 80 to 100 small burns on the trabecular meshwork. The exact mechanism by which argon laser trabeculoplasty works is not known, but the procedure is initially effective in almost 80% of patients. Unfortunately, at 5 years almost 50% of patients who initially responded to the laser are no longer controlled. A prospective study of 203 patients demonstrated that argon laser trabeculoplasty as the initial treatment was equally efficacious as medical therapy[2] and does diminish the systemic risks by reducing the medications needed.
[edit] Surgery
The IOP can be effectively controlled with glaucoma filtration surgery, in which a fistula is created between the anterior chamber and the subconjunctival space. The procedure is 85% to 90% effective but does carry significant potential complications, including cataract formation. When successful, the procedure may reduce or eliminate the need for glaucoma medications and does not depend on the compliance of patients with their medications. In the United States surgery is done when medications and lasers are not effective. The Scottish Glaucoma Trial and the Moorfields Primary Treatment Trial showed lower pressures and better visual fields when surgery was used as the initial intervention.[3] An NIH trial is currently underway to study this question as well.
Much of the success of modern glaucoma surgery can be attributed to the use of the antimetabolites 5-fluorouracil and mitomycin, which in prospective clinical trials showed substantial improvement in surgical success in high-risk cases.[4] They prevent scarring of the fistula. However, the poorly healed fistula may serve as an entry portal for bacteria, and as many as 8% to 10% of these patients may be at serious risk for developing an intraocular infection (endophthalmitis) over their lifetime. Therefore even a simple conjunctivitis should be treated as a significant medical emergency for a patient who has had glaucoma surgery.
[edit] SPECIAL ISSUES
[edit] Preoperative and Postoperative Surgical Management
The glaucoma patient may be sent to a general practitioner before glaucoma filtering surgery for medical evaluation. Unlike cataract surgery, these procedures are often not elective, and prolonged delays may be vision threatening.
The surgery may be done under local anesthesia, particularly in elderly patients with significant cardiovascular and/or pulmonary disease. Lidocaine (Xylocaine) and bupivacaine (Marcaine) are often used for regional blocks, and epinephrine may be added for hemostasis and prolongationof the block. Allergies to these medications need to be noted, and contraindications to epinephrine use need to be explicitly conveyed to the operating surgeon.
Occasionally, general anesthetics are used. A particular problem arises if the patient has been using long-acting parasympathomimetics such as echothiophate iodide (Phospholine Iodide) to control glaucoma. If succinylcholine is used as a paralyzing agent during intubation, there may be prolonged apnea because of the pseudocholinesterase inhibition by the echothiophate. In addition, succinylcholine may also cause a transient rise in IOP due to sustained extraocular muscle contraction.
Since vascular disease is one of the risk factors in glaucoma, it is not surprising that some of these patients may be taking anticoagulation medication. Anticoagulation can create several problems during glaucoma surgery, including a retrobulbar hemorrhage during the local block and an increased risk of an intraoperative sudden massive hemorrhage from a suprachoroidal blood vessel, which usually results in blindness. Therefore, if possible, anticoagulation medications such as aspirin and Coumadin should be discontinued, if medically safe, before surgery. The IOP may be very low for several days following the surgery, and the anticoagulation medications can be safely restarted once the IOP returns to the normal range.
Close attention needs to be taken to control systemic hypertension and to suppress severe coughing during the procedure. Identifiable sources of infection such as an active upper respiratory tract infection need to be cleared if possible before surgery.
Postoperatively, patients often have very blurred vision until the IOP stabilizes. The eye is often patched or covered with a protective metal shield, and care needs to be taken to avoid falls. Strenuous activity such as heavy lifting should be avoided. Other activities such as a physical rehabilitation program might need to be modified for a limited time, and employed individuals may request temporary disability because of their blurred vision and the limitation of activity that is required during their convalescence.
[edit] REFERENCES
- ↑ 1.0 1.1 A Sommer, J Tielsch, J Katz,et al.: Racial differences in the cause-specific prevalence of blindness in East Baltimore. N Engl J Med 1991; 325:1412 - 1417.
- ↑ Glaucoma Laser Trial Research Group: The Glaucoma Laser Trial (GLT) and Glaucoma Laser Trial Follow-up Study: 7, Results. Am J Ophthalmol 1995; 120:718 - 773.
- ↑ C Migdal, W Gregory, R Hitchings: Long-term functional outcome after early surgery compared with laser and medicine in open-angle glaucoma. Ophthalmology 1994; 101:1651 - 1657.
- ↑ The Fluorouracil Filtering Surgery Study Group: Five-year follow up of the fluorouracil Filtering Surgery Study. Am J Ophthalmol 1996; 121:349 - 366.
