Ординатура / Офтальмология / Английские материалы / Clinical Pathways in Glaucoma_Zimmerman, Kooner_2001

other agents when combined with them, such as the phenothiazines and the antidepressant agents mentioned above. Specifically, the agents phenelzine sulfate59 (Nardil) and tranylcypromine sulfate59 (Parnate) have been shown to be associated with episodes of angle-closure glaucoma.

What Is the Role of Mood-Altering Agents,

such as Minor Tranquilizers, Sedatives, and Stimulants?

This is a rather diverse class of agents including sedatives such as diazepam (Valium), morphine, barbiturates, stimulants such as amphetamine, and the methylxanthines such as caffeine and theophylline. Although Valium was reported to have been taken by a patient having an attack of angle-closure glaucoma,65 this finding was refuted subsequently in the literature,66 due to the lack of any known effect of Valium upon the eyes. Barbiturates, morphine, paraldehyde, meperidine, reserpine, and phenytoin have not been reported to produce an elevated IOP.

The amphetamines have not been documented in the literature to have produced an elevated IOP in any patient.

The methylxanthines are a rather large and diverse group of agents and can be found in a great variety of agents including the above-mentioned caffeine and theophylline as well as chocolate! Although no reported cases of glaucoma have been reported with these agents, I was recently referred a case of medically uncontrolled open-angle glaucoma. This patient, a 54-year-old black woman on maximal medical therapy, had an IOP of 35 mm Hg in both eyes and optic nerve damage per funduscopy in both eyes. The only remaining positive history was that she was a heavy coffee drinker, by her estimate, having 19 cups of black coffee daily. I immediately prescribed the elimination of all caffeine from her diet, and within 24 hours the IOP was 19 mm Hg in both eyes. On all follow-up visits the patient was caffeine free, and the IOP has been within normal limits—under 21 mmHg. The mechanisms of action to produce an elevated IOP in this case is poorly understood at this time and may be related to the ability of the methylxanthines to block the enzyme phosphodiesterase and to increase intracellular levels of cyclic adenosine monophosphate67 (cAMP), in contrast to the effect of the -adrenergic agents such as timolol.68

What Is the Role of Antibiotics?

SULFA DRUGS

The sulfa drugs have been well documented to produce an idiosyncratic swelling of the lens associated with shallowing of the anterior chamber, retinal edema, and elevated IOP.69 These episodes do not involve the pupil and are not responsive to cycloplegic agents, resulting in the present thinking that these cases reflect an idiosyncratic response of the lens to sulfa agents.70 This observation has been confirmed by A-scan measurements of the eye during such an attack.71 Some authors feel that the response of the lens to these agents reflects an acute swelling of the ciliary body, resulting in marked zonular relaxation and the subsequent swelling of the lens observed in these cases. This phenomenon

342 Drug-Induced Glaucoma

has been observed when sulfa has been used in a variety of agents including antibiotics69 and antihypertensive agents (e.g., hydrochlorthiazide)72 and as carbonic anhydrase inhibitors (e.g., acetazolamide).73

QUININE

This phenomenon has also been reported to produce an elevated IOP with quinine.74

TETRACYCLINE

Tetracycline has also been documented to produce an idiopathic swelling of the lens.75

What Is the Role of Antiparkinsonian Agents?

The antiparkinsonian agents act through two mechanisms: (1) replenishing diminished stores of dopamine in the corpus striatum, and (2) acting as a strong anticholinergic. It is those agents in the latter category that we are concerned with. Indeed, trihexyphenidyl HCl76 (Artane) has been documented to precipitate angle-closure glaucoma. This finding is felt to reflect the anticholinergic action of this agent.76

What Is the Role of Antispasmolytic Agents?

These agents act to reduce both the gastric secretion and the motility of the stomach. Their action directly reflects their anticholinergic power. Although no attacks of angle-closure glaucoma have been documented with these agents, propantheline bromide77 (Pro-Banthine) and dicyclomine HCl77 (Bentyl) have been documented to raise the IOP in patients with open-angle glaucoma. This effect is felt to reflect their anticholinergic action.

What Is the Role of Anesthetic Agents?

General anesthesia has always entailed increased risk to the patient, including the risk of elevated IOP and glaucoma. It has always been difficult to separate the various risk factors to the patient undergoing general anesthesia. The induction of general anesthesia itself may be associated with an elevated IOP from laryngeal spasm, coughing, and wheezing associated with endotracheal intubation.78 Although this is a significant risk to the patient with an open globe, what we are most concerned with are those factors introduced by the physician/anesthesiologist at the time of surgery.

Specifically, succinylcholine,79,80 ketamine,81 and chloral hydrate82 have been well documented to raise IOP. This effect is felt to be due to increased extraocular muscle tone from these agents.83

The preoperative use of atropine, scopalmine, and ephedrine has been felt to be associated with attacks of angle-closure glaucoma following general anesthesia.84–86

Although many factors may be out of the hands of the surgeon and/or anesthesiologist, careful screening of preoperative and intraoperative medications may help to minimize this risk to patients.

What Role Do Surgical Agents Play

in Inducing Glaucoma?

VISCOELASTIC AGENTS

Hyaluronic acid (Healon) and sodium chondroitin sulfate have been developed to protect the corneal endothelium at the time of intraocular surgery. Both of these agents have been associated with an elevated IOP in the immediate postoperative period.87,88 This elevated IOP is felt to directly reflect an acute obstruction of the trabecular meshwork outflow channels and is usually seen within 12 to 24 hours after surgery.89 Although there was some initial feeling that this finding reflected the large molecular weight of these agents, it has also been observed to occur when a low molecular weight substance is used.90 It is my observation that if these agents are carefully washed out of the eye at the time of surgery, a great deal of these problems will be avoided in the immediate postoperative period.

SILICONE OIL

This agent has become popular during pars plana vitrectomy and the repair of complicated retinal detachments. Silicone oil has been associated with attacks of elevated IOP.91 The silicone oil may emulsify, forming bubbles that may clog the trabecular meshwork.92 In addition, pupil block glaucoma93 may also be observed to occur in these patients. This effect is felt to be due to occlusion of the pupil with silicone oil producing iris bombé and acute angle-closure glaucoma.93 The treatment may vary from a simple washout of the silicone oil from the anterior chamber to a surgical filtering procedures.94 In the patient at risk for angle-closure glaucoma, an inferior peripheral iridectomy is recommended.93

What Role Do Antihistamines Play

in Inducing Glaucoma?

The antihistamines are a diverse group of agents that can be broadly broken down into two classes—the H1 and the H2 antihistamines. The H1 antihistamines block the action of histamine on capillary permeability and vascular, bronchial, and other smooth muscles. The H2 antihistamines also block the effect of histamine on the smooth muscles of the peripheral blood vessels and the secretion of gastric acid. What makes this group of importance is the anticholinergic action of these agents. Although the anticholinergic action is mild, orphenadrine citrate (Norgesic),95 an H1 antihistamine, has been documented to have precipitated an attack of angle-closure glaucoma. The H2 antihistamines cimetidine and ranitidine have been documented to raise the IOP in one patient with glaucoma being treated for a duodenal ulcer.96 This effect has not

344 Drug-Induced Glaucoma

been repeated by other authors. It should also be noted that the H1 antihistamine promethazine HCl (Phenergan) has been shown to produce an idiopathic swelling of the lens as documented with the sulfa agents.97 Although the action of these agents on the whole is rather weak, they should be approached with caution in the patient at risk for glaucoma.

What Role Do Autonomic Agents Play

in Inducing Glaucoma?

SYMPATHOMIMETIC AGENTS

This class of agents has generally been associated with the treatment of glaucoma, through their ability to dilate the pupil, but they may precipitate attacks of angle-closure glaucoma68,99 and raise the IOP in patients with open-angle glaucoma98 (Table 15–5). This is important because these agents are found in a wide variety of products including inhalers used for the treatment of asthma and in rectal suppositories.

PARASYMPATHOLYTIC AGENTS

All of these agents have a marked propensity to dilate the pupil and place the susceptible patient at risk for an attack of angle-closure glaucoma. These agents are found in a wide variety of products from timed-release discs for the treatment of motion sickness (Transderm-Scop)101 to a variety of inhalers used for the treatment of asthma. These products should be used with caution in the susceptible patient (Table 15–6).

What Role Do Inhalation Agents Play

in Inducing Glaucoma?

As mentioned above, a wide variety of agents are found in inhalation products, including the sympathomimetic and parasympathomimetic agents. In addition, salbutamol102 and ipratropium103 have also been documented to precipitate attacks of angle-closure glaucoma. This action is felt to be due to the anticholinergic action of ipratropium in combination with the effect of salbutamol on aqueous humor production.104 These agents should be used with caution in the patient at risk for such an attack of glaucoma.

Table 15–5. Sympathomimetic Agents and Glaucoma

Epinephrine68*,98+

Ephedrine99*

Phenylephrine68*,98+

Hydroxyamphetamine99*

*Narrow-angle glaucoma. +Open-angle glaucoma.

Table 15–6. Parasympatholytic Agents and Glaucoma

Cyclopentolate (Cyclogel)99,100

Tropicamide (Mydriacil)68,100

Atropine (Atropisol)68,100

Homatropine Hydrobromide68,100

Scopalomine (Transderm V, Hyoscine)68,100

What Role Do Cardiac Agents Play

in Inducing Glaucoma?

The traditional cardiac agents including digitalis and quinidine do not appear to have any effect on the IOP. However, interestingly, disopyramide phosphate (Norpace)105 does appear to have some anticholinergic activity and has indeed been documented to produce an attack of angle-closure glaucoma. Newer agents including the calcium channel blockers have been shown to have mixed results on the IOP at this time.106,107

What Is the Role of Botulinum Toxin (Oculinum)?

Botulinum toxin has become popular for the treatment of essential blepharospasm and ocular muscle palsy. This injectable agent has been documented to produce an acute attack of angle-closure glaucoma.108 The mechanism of action for this is felt to be the effect of this drug on the ciliary ganglion, producing pupillary mydriasis.109

What Is the Role of Aspirin (Acetylsalicylic Acid)?

Aspirin has been reported to produce an idiopathic swelling of the lens in association with an elevated IOP.110 The patient with narrow and/or occludable angles should be cautioned about the use of aspirin.

What Is the Treatment

of Nonsteroidal Drug-Induced Glaucoma?

The initial consideration is whether the patient can stop using the offending agent (Fig. 15–4). In many cases, the simple removal of the precipitating agent may be enough to successfully treat the patient. Unfortunately, in many cases, considerable damage may have already occurred, and the patient may need to be treated in the traditional fashion of the patient with glaucoma (Fig. 15–4).

In other patients the offending agent is medically necessary and cannot be stopped without placing the patient at undue risk. In these cases the patient is treated similarly to the patient initially presenting the clinician with traditional glaucoma (see Fig. 15–4). The difficulty in these cases is that with the offending agent still being used, medical therapy is often unsuccessful, requiring more aggressive treatment, including surgery (Fig. 15–4).

346 Drug-Induced Glaucoma

Figure 15–4. Algorithm for management of noncorticosteroid drug-induced glaucoma.

What Is the Key to Successful Treatment?

Overall, the key to successful treatment in all of these patients is time and consideration by the clinician to carefully determine the role that these agents play in the patient’s glaucoma.

Future Considerations

What Is New in Drug-Induced Glaucoma?

There is a lot of interest in the question of steroid regulation of trabecular meshwork induced glucocorticoid response protein (TIGR).111 Topical application of anecortave acetate (AL3789) reduced IOP in glucocorticoid-induced ocular hypertension in rabbits and in humans.112

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