Glaucoma and the Primary Care Physician
Glaucoma and the Primary Care Physician
Author: Izak F. Wessels, MD, FRCSE, FRCOphth, FACS, Associate Professor, Department of Ophthalmology, Chattanooga Unit, College of Medicine, University of Tennessee.
Peer Reviewer: Paul Y. Chung, MD, Assistant Professor of Ophthalmology, Loma Linda University School of Medicine, Chief, Opthalmology Section at VA Medical Center, Loma Linda, Calif.
Editor’s Note—Glaucoma describes a family of different disease entities associated with progressive visual field loss and atrophy of the retinal ganglion cells and nerve fiber layer, with excavation of the optic disc. On average, one in 25 persons aged 50 or older will have glaucoma; less than one half of those will have been diagnosed or received treatment. In African Americans glaucoma occurs 2-4 times more commonly, and the disease also progresses more rapidly. Tragically, the diagnosis is too often made only after extensive damage has occurred and there is no possibility of restoring what has been lost. The primary care physician (PCP) is likely to encounter patients with glaucoma, since the indolent nature of this disease does not result in self-referral. Therefore, a high index of suspicion, basic understanding of mechanism of the disease and awareness of the more obvious signs will facilitate appropriate management.
This article attempts to improve glaucoma awareness, as well as provide such important practical points as are relevant to the PCP. The first point includes being able to assess an anterior chamber for depth and performing palpation to detect severely elevated pressure in acute angle closure. The next two include evaluating the optic nerve and awareness of the pattern of visual field loss in glaucoma. Visual field loss is often on the side toward the opposite eye. PCPs should be aware that a pressure measurement can be normal in glaucomatous eyes. Medication effectiveness can be improved by nasolacrimal occlusion. Awareness of the categories of medications, their side effects, and the important interactions with other conditions particularly emphasizes the common side effects that must be recognized and monitored by the PCP. PCPs should be aware of the different surgical options for glaucoma. Some of the common surgical procedures are briefly listed, noting those elements important to the PCP.
Introduction
Glaucoma is not defined by a specific intraocular pressure but rather as an optic neuropathy that can occur at any intraocular pressure depending on the optic nerve susceptibility of the individual person. Treatment effectively prevents progression, if the appropriate medication has been selected, the patient complies well, and where necessary, judicious surgical intervention is performed in a timely manner.
Glaucoma is a leading cause of blindness worldwide, and is estimated to result in more than 6 million bilateral blind people in the year 2000.1 This paper will review three clinically important types of glaucoma. The first is closed angle glaucoma. Although uncommon, it may present as a medical emergency. Every PCP should be able to use simple evaluations to exclude this condition. The next is congenital glaucoma. While this condition is extremely rare, it must not be overlooked, since early diagnosis and treatment are critically important for visual function. Finally, most emphasis will be placed on the prevalent chronic open angle glaucoma.2,3
The practical points presented (anterior chamber depth, palpating for grossly elevated pressure, and recognizing the classic optic disc changes with a direct ophthalmoscope) lie well within the scope of physicians and nurse practitioners.4,5 Traditionally, ophthalmologists have diagnosed and treated glaucoma both medically and surgically. More recently, the scope of practice of optometrists has expanded in most (but not all) states to include the diagnosis and medical treatment of glaucoma. They can be a valuable resource to the PCP for evaluating, selecting, and implementing therapy, as well as follow-up and appropriate referral for surgery.
Acute angle closure glaucoma. This is a distinctly uncommon disease, except in specific ethnic groups.6,7 Nevertheless, patients with an acute attack may present first to a PCP. The usual complaint is that of one eye spontaneously becoming excruciatingly painful, with blurred vision and haloes around lights.8 There is a mid-dilated, poorly responsive pupil, hazy cornea, and diffused corneal light reflex (due to the corneal edema scattering the reflection, as if the cornea is covered with fine dewdrops), all due to the markedly elevated pressure.9
Useful confirmatory tests include noting the depth of the anterior chamber (the distance between the cornea and iris) and whether the iris is bowed forward. By shining a light across the eye from the side, the normally flat iris is uniformly illuminated; any forward bowing will result in illumination only on the side of the iris closest to the light. The iris lying on the other side of the pupil will appear to be in a shadow (see Figure 1). Furthermore, by gently palpating the eye through the closed upper lid (see Figure 1), the markedly elevated pressure will be quite obvious.
Certain individuals are at higher risk: females 3:1 compared to males, those older than 55, those with autosomal dominant inheritance, those with Eskimo or Asian ancestry, those with farsighted eyes (hyperopia), and patients with a smaller than normal cornea.6 Because a markedly elevated intraocular pressure stimulates the oculocardiac reflex (via the vagus nerve) other findings include bradycardia, dizziness, nausea, and frequently, vomiting. These findings might mislead the PCP to consider an acute intra-abdominal problem, while the ocular symptoms may be overlooked.10 It is common to treat acute angle closure glaucoma with virtually all pressure lowering medications, including beta blockers and alpha agonists. Ignoring the problem can result in irreversible blindness after just a few hours. Immediate, urgent referral is necessary, and treatment includes systemic (IV or PO) acetazolamide (diamox); aqueous suppressants and miotic drops (£ 2% pilocarpine); and placing the patient in a supine position to allow the iris to fall back from the anterior chamber angle and permit the fluid to drain. Parenteral (mannitol) and oral (glycerol) hyperosmotic agents also may be required.11 Certainly, the definitive treatment is a peripheral iridotomy, and the sooner it can be performed the better.
Note that the common labeling on medications as "not for use in glaucoma" applies only to angle closure cases, in which anticholinergic side effects can provoke pupil dilation and result in angle occlusion. Patients with the far more common open angle glaucoma need not be concerned. Primary open angle glaucoma and acute glaucoma are totally different in pathogenesis, symptoms, and treatment.
The symptoms and signs of acute glaucoma are so characteristic that recognition usually is easy and treatment can be begun early enough to prevent permanent angle damage and secondary glaucoma. Secondary angle closure may occur after vascular insult to retina, also as a complication of severe diabetic retinopathy.
Pediatric glaucoma. Pediatric glaucoma, although exceedingly rare, should be readily apparent due to markedly enlarged corneal diameters: the immature infant eye stretches when there is elevated intraocular pressure, but this may be overlooked if the disease is bilateral. If detected early, the optic nerve may recover.11 Parents may notice the light sensitivity due to swelling of the cornea, as well as persistent tearing; the latter symptom should not be mistaken for the far more common cause of a congenitally obstructed nasolacrimal duct.
Open angle glaucoma. Previously known as chronic simple glaucoma, primary open angle glaucoma is asymptomatic until late in its course, and appropriate screening by PCPs can greatly help reduce the incidence of irreversible visual loss.13-15 Glaucoma is common, even more so in African Americans.3 Not every patient needs to be treated: the life expectancy, functional ability, and ocular health in general can guide therapy.16,17 The progression is exceedingly slow; simply by being under treatment seems to result in fewer problems. Glaucoma case finding is feasible in general practice.18-21 Direct ophthalmoscopy proved to be the most valuable single test in diagnosing glaucoma, and the combination of measurement of intraocular pressure and direct ophthalmoscopy was shown to be the most likely method of diagnosing glaucoma or identifying glaucoma suspects.9,19,20
Other methods of identifying the disease include a questionnaire-based algorithm for detection of overall eye disease, with a relative sensitivity/specificity of 90%/44%; determining decreased distance visual acuity (£ 20/40), 61%/72%; dilated fundus examination, 79%/82%; tonometry, 27%/96%; and supra-threshold visual field testing, 70%/67%.20 This indicates that fundus examination has the highest sensitivity and specificity.
The intraocular pressure plays an important role, despite the absence of a specific number distinguishing between disease and health.4,16,22 A severely elevated pressure can result in vascular occlusion, but even mild elevation can, over years, be associated with progressive damage. While there is not an absolute level above which glaucoma can be diagnosed, lowering the pressure can delay or prevent visual loss. This finding has facilitated treatment that varies from close observation to topical and systemic medications. Attempts to improve the fluid flow and drainage include: openings to bypass obstructions (e.g., peripheral iridotomy that can be curative for narrow angle glaucoma) and improve fluid drainage (goniotomy for congenital glaucoma, laser trabeculoplasty, and trabeculectomy for open angle glaucoma); implanting a device to improve drainage; and laser or cryo-ablation of the secretory structures.11
Diagnosis
Four parameters together help make the diagnosis vision, evidence of typical glaucomatous field loss, optic nerve cupping, and intraocular pressure.20,23
Visual field loss. Modern, computerized test devices permit measuring the visual field more quickly and consistently than is possible with manual methods. Unfortunately, the field loss is not that specific or sensitive and usually only detects damage that is relatively far advanced. Most PCPs test the peripheral field for driving requirements by evaluating how far the field extends out temporally in each eye. Often, the first area of the visual field to suffer loss lies on the nasal side, while the other eye (usually with asymmetric and nonoverlapping field loss) will have good function. Moreover, the onset and progression is so gradual as to be imperceptible until it is extremely advanced.24
The optic disc contour. Practitioners routinely use the direct ophthalmoscope to evaluate the optic nerve (for papilledema, optic atrophy, as well as for glaucoma). It helps to be familiar with the appearance of a normal disc (see Figure 1). This recognition can best be achieved by routine use of the ophthalmoscope on all patients, including normals.25 Several specific findings should be noted.
The optic nerve head shows an increase in the area occupied by the optic cup. (See Figure 2.) The extreme case is obvious (see figure 3), but obviously it is best to suspect the disease before irreversible visual field loss has occurred. Early signs include vertical enlargement of the cup, a focal area of thinning of the rim. Ultimately, the vessels become displaced nasally, and "bayonet" as they dip under the rim after crossing.
Flame shaped hemorrhages on the disc margin are markers for more rapid visual field loss. (See Figure 2.)
The astute observer may notice a loss of the normal nerve fiber layer sheen adjacent to the disc. The nerve fiber layer is more noticeable when using the green filter on the ophthalmoscope. (See Figures 2 and 3.)
Specific findings indicating a greater risk for damage include large nerves, peripapillary atrophy, and prominent laminar dots.22,26 While the appearance of the disc alone is not sufficient to make the diagnosis, its evaluation is critically important. The ability to appropriately evaluate an optic disc is greatly facilitated by a brief training course.12,13,19
Intraocular pressure. The frequency of distribution (histogram) of intraocular pressures in the general public is a skewed bell curve.11 Normal pressure is considered as 17 mmHg, with two standard deviations (i.e., 95% of the sample included), including 12-22 mmHg. Only 10% of patients with pressures above 24 will develop glaucoma; but with higher pressures, the risk increases (50% will develop damage if the pressure is > 27 and almost all will have damage if the pressure remains > 30 after 15 years). In eyes with glaucoma the mean pressure is only 23, while one-third will have pressures in the "normal" range. The intraocular pressure varies during the day (usually highest in the morning), and requires relatively expensive delicate instruments as well as meticulous technique to measure the pressure.
There is, indeed, no single diagnostic procedure to give a "yes" or "no" answer. The intraocular pressure is nothing more than a significant risk factor.2 While pressure measurements are important for follow up and management, the PCP should not rely on pressure measurements alone for diagnosis. The PCP has a special role in encouraging those on glaucoma medications to comply with their medication use. Since there are no obvious signs of benefit, compliance is a major problem, more so since medication does not cure but only preserves what remains.27
Medical Treatment
The goal of therapy is not simply to lower the pressure in the eye.28 The patient in whom the disease does not appear to be rapidly progressing, and who is without much functional disability and has a relatively short remaining lifespan, should not receive drastic treatment. Consideration must be given to not worsen the overall well being of the patient, especially because glaucoma medications have numerous side effects.27-29 However, noncompliance remains a major problem, and surgical intervention may be required to prevent visual loss.
The newer agents are extremely potent, with many potential interactions as well as serious systemic side effects.29 It is not commonly realized that eye drops are extremely concentrated.30 Timolol 0.5% in each mL contains the same dose as a 5 mg tablet. Each milliliter usually produces an average of 20 drops; therefore, a daily dose of one drop in each eye will deliver 0.5 mg, which can result in toxic systemic levels in the case of a child. In susceptible adults, this drug may cause bronchospasm, reduced exercise tolerance, fatigue, impotence, and even congestive heart failure.
Nasolacrimal punctal occlusion is a beneficial technique to reduce side effects by minimizing systemic absorption of the drops.27 The patient puts a clean finger over the nose where the upper and lower lids meet and pushes directly onto the bone. Then they instill the drop (usually an assistant is needed) and gently close the lids, without forcible blinking. To achieve a good effect, they should remain thus for 3 minutes or longer. By this simple maneuver, the amount of drug entering the nose is drastically reduced. The nasal mucosa would otherwise allow immediate absorption directly into the systemic circulation. Lacrimal occlusion also markedly increases the contact time with the eye and a higher dose can be delivered, allowing a reduction in the frequency of instillation without noticeable loss of effect.
Categories of Medications
Parasympathomimetics. Pilocarpine, carbachol, and others all act directly on the muscarinic receptors to cause contraction of the muscles of the ciliary body, which may open the drainage meshwork to increase outflow. They also cause pupil constriction (and headache), while other cholinergic side effects (diarrhea and gastrointestinal upset) may occur. A subclass of indirect parasympathomimetics acts by inhibiting acetylcholine esterase. While only rarely used now, the PCP should be aware of their potentiation of the effects of succinyl choline (scoline) muscle relaxants. Furthermore, all parasympathomimetics can worsen inflammation (uveitis) and may increase retinal detachment risk.
Adrenergic sympathomimetics. Epinephrine was at one time used frequently, but has been replaced by a prodrug dipivefrin (Propine) that only becomes activated within the eye. Known side effects include aggravation of hypertension, thyrotoxicosis, and interactions with MAO inhibitors. More specific alpha agonists have become available, including apraclonidine (Iopidine) and brimonidine (Alphagan). These agents may cause side effects due to interaction with MAO inhibitors, or in patients with liver or kidney impairment. The sympathomimetic effect can obviously provoke or worsen problems such as Raynaud’s phenomenon, thromboangiitis obliterans, or symptoms due to coronary or cerebral artery disease.
Beta-blockers. These drops are used more frequently than almost all the other drugs put together.31 There are numerous agents available, both selective and nonselective.32 They often have systemic side effects (loss of exercise tolerance, impotence, elevation of blood lipids, bradycardia, cardiac arrhythmias, bronchospasm, depression, etc.) that may be overlooked as due to other factors. Other signs include worsening of chronic obstructive pulmonary disease; reactive airway disease; bradycardia; heart block; heart failure; myasthenia gravis; depression; and interaction with digitalis, quinidine, and reserpine.
Carbonic anhydrase inhibitors. These can also cause significant side effects, ranging from a metallic taste to lethargy, weight loss, poor appetite, nausea, and GI upset. Other, more serious problems include renal impairment, calcium kidney stones, and hypokalemia that obviously will potentiate digitalis toxicity. Patients who are allergic to sulfonamides can suffer from catastrophic Stevens Johnson syndrome and aplastic anemia. Even those without sulfa allergies may develop aplastic anemia. These agents can increase the effect of aspirin.
Prostaglandins. Latanoprost (xalatan) is extremely potent; therefore, the medication is dilute, but the cost is high. It functions by increasing uveoscleral absorption and thus increases aqueous absorption through a different pathway than the trabecular meshwork. Frequent side effects range from an allergic conjunctivitis to permanent darkening of light brown/green colored irides. Being a prostaglandin analog, it may aggravate ocular inflammation (uveitis, cystoid macular edema, etc.).
Since each drug has a particular benefit as well as relative contraindications, the selection and prescription is beyond the scope of this brief review. While it is important for the PCP to have some knowledge of the potential interactions, the choice and prescription would best be left to those practitioners familiar with these agents.
Surgery
There is a range of different surgical options, the precise indications and techniques of which are less important to the PCP than an awareness of potential complications.
Laser trabeculoplasty. A blue-green laser is used to place mild burns just in front of the filtration area on the inside of the cornea peripherally. The burns decrease the resistance to outflow and consequently the pressure decreases. While usually only effective for a few years, it can minimize or avoid totally the need for medications temporarily.33
Table 1. Details of Complaints Reported During Treatment (Glucosamine) | |||
Category | Effect | Side Effects | Interactions |
Parasympathomimetics | Increase outflow (note: these drops usually have a green cap) | Succinyl choline | |
Pilocarpine | pupil constriction, GI upset | ||
Carbachol | inflammation (uveitis), | ||
retinal detachment | |||
Phospholine Iodide | brow ache (due to spasm of ciliary muscle) | ||
Adrenergic drugs | Increase aqueous outflow | MAO inhibitors | |
Epinephrine | aggravation of hypertension, | ||
Dipivefrin (Propine) | thyrotoxicosis | ||
Alpha agonists | Decrease aqueous production | ||
Apraclonidine (Iopidine) | liver kidney impairment | ||
Brimonidine (Alphagan) | Raynaud's phenomenon, | ||
thromboangiitis obliterans, and | |||
coronary or cerebral artery disease | |||
Beta-blockers | Decrease aqueous production | Quinidine, reserpine, | |
Timolol (Timoptic) | impotence | digitalis | |
Betaxolol (Betoptic) | elevation of blood lipids | ||
Levobunolol (Betagan) | bronchospasm COPD reactive airway disease | ||
Metipranolol (Optipranolol) | myasthenia gravis | ||
Carteolol (Ocupress) | bradycardia, heart block, heart failure | ||
depression, and loss of exercise tolerance | |||
Carbonic Anhydrase inhibitors | Decrease aqueous production | ||
Oral | |||
Methazolamide (Neptazane) | renal impairment | sulfa allergy | |
Acetazolamide (Diamox) | calcium kidney stones, | aspirin | |
hypokalemia | digitalis | ||
Topical | |||
Dorzolamide (Trusopt) | |||
Brinzolamide (Azopt) | |||
Prostaglandins | Increase outflow through | ||
uveoscleral pathway | |||
Latanoprost (Xalatan) | allergic conjunctivitis; | ||
permanently darken a light iris, | |||
cystoid macular edema, uveitis |
Trabeculectomy. This surgery is the most often performed glaucoma surgery, and is used to create an alternative pathway with reduced resistance to flow. After lifting the conjunctiva, a partial thickness flap of sclera is dissected, followed by removing the remaining tissue holding the aqueous back. When the partial thickness outer flap is repositioned, the aqueous fluid now only has to traverse the thinner flap, and it usually more easily percolates through to collect under the conjunctiva and be absorbed. Currently, anti-fibrotic agents (e.g., mitomycin C, 5 Fluoro uracil) are used to prevent the flap from scarring down and blocking the outflow. Often, a thin-walled bleb develops at the site of a successful trabeculectomy surgery. This thin area (obviously visible as an avascular fluid filled vesicle) can sometimes permit infectious organisms to easily penetrate the eye and produce a severe infection. PCPs should be able to recognize the presence of the bleb under the eyelid, and more aggressively manage even minor conjunctivitis in these high-risk patients.
Drainage tubes. In cases with marked scarring, or in whom trabeculectomies have failed, a permanent plastic tube can be implanted into the anterior chamber to help the aqueous fluid leak out. Various devices are commercially available, each named after its inventor, e.g., Ahmed, Molteno, Baerveldt, etc.
Ciliary ablation. The aqueous fluid is produced by the ciliary body, and glaucoma results from production exceeding absorption. As a corollary to increasing the absorption of the fluid, it is logical to attempt to surgically reduce the production. Any damage to the ciliary body will result in a reduction in inflow and intraocular pressure. Cryotherapy or laser surgery can ablate the ciliary body and effectively reduce the pressure, although the magnitude of effect is difficult to control.
Summary
There are several points of importance for the PCP.
Acute closed angle glaucoma often presents as an emergency (frequently with symptoms apparently originating elsewhere). The shallow anterior chamber and palpably elevated intraocular pressure is very helpful. Peripheral iridotomy is curative.
Glaucoma can occur in children.
Open angle glaucoma is a common disease that lacks a specific diagnostic test. There is no red line for the intraocular pressure. Measuring the pressure accurately is not simple, and the reading must be interpreted in the light of the visual field test and the contour of the optic nerve head.34
Changes of the optic nerve (increased cupping, bleeding on the margin, and loss of thickness of the rim) will frequently present to the PCP. Like most other skills, it becomes easier to recognize abnormalities with practice. Screening for glaucoma ought to be part of every general medical practice.35,36
Glaucoma medicines are potent, and frequently cause patients to present to the PCP with side effects. Furthermore, other medications can interact with glaucoma: e.g., systemic corticosteroids may elevate the intraocular pressures and cause glaucomatous damage in the 5% of genetically predisposed individuals.
Early referral to a qualified optometrist or ophthalmologist is strongly recommended to facilitate timely treatment.37,38 Consultation with suitably qualified optometrists (certain states) may facilitate management.
Surgical treatment can be successful. However, the eye may be at significant risk for endophthalmitis due to a thin (conjunctiva only) and often avascular layer separating the organisms on the conjunctiva from the inside of the eye.
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