Ординатура / Офтальмология / Английские материалы / Clinical Pathways in Glaucoma_Zimmerman, Kooner_2001
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Figure 21–1. Suggested algorithm for management of POAG in pregnancy.
tinues to be challenging due to poorly defined risks. However, this uncommon clinical dilemma appears to attract little attention among glaucoma investigators, and it is anticipated that progress in this area will remain slow.
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References
1.Leske MC, Connell AMS, Wu SY, et al: Risk factors for open-angle glaucoma. Arch Ophthalmol 1995;113:918.
2.Goldwyn R, Waltman SR, Becker B: Primary open-angle glaucoma in adolescents and young adults. Arch Ophthalmol 1970;84:579–582.
3.Mandell AI, Elfervig J: Open-angle glaucoma in patients under forty years of age. Perspect Ophthalmol 1977;1:215.
4.Cunningham FG, MacDonald PC, Gant NF, et al. Williams’ Obstetrics, 20th ed. Stamford: Appleton & Lange, 1997;693.
5.Wilensky JT: Pregnancy and glaucoma. In: Higginbotham EJ, Lee DA (eds): Management of Difficult Glaucoma. Boston: Blackwell Scientific, 1994;246–249.
6.Kooner KS: Personal communication/unpublished observations.
7.Kearns PP, Dhillon BJ: Angle closure glaucoma precipitated by labour. Acta Ophthalmol 1990;68:225–226.
8.Kahn HA, Leibowitz HM, Ganley JP, et al: The Framingham Eye Study. II. Association of ophthalmic pathology with single variables previously measured in the Framingham Eye Study. Am J Epidemiol 1977;106:33.
9.Leske MC, Podgor MJ: Intraocular pressure, cardiovascular risk variables, and visual field defects. Am J Epidemiol 1983;118:280–287.
10.Leighton DA, Phillips CI: Systemic blood pressure in open angle and low tension glaucoma and normals. Br J Ophthalmol 1972;56:447–453.
11.Qureshi AI, Xi XR, Wu XD: Intraocular pressure trends in pregnancy and in third trimester hypertensive patients. Acta Obstet Gynecol Scand 1996;75:816–819.
12.Phillips CI, Gore SM: Ocular hypotensive effect of late pregnancy with and without high blood pressure. Br J Ophthalmol 1985;67:117–119.
13.Armstrong JR, Daily RK, Dobson HL, et al: The incidence of glaucoma in diabetes mellitus: a comparison with the incidence of glaucoma in the general population. Am J Ophthalmol 1960;50:55.
14.Becker B: Diabetes mellitus and primary open angle glaucoma. The XXVII Edward Jackson Memorial Lecture. Am J Ophthalmol 1971;71:1.
15.Klein BE, Klein R, Moss SE: Intraocular pressure in diabetic persons. Ophthalmology 1984;91:1356.
16.Sunness JS: The pregnant woman’s eye. Surv Ophthalmol 1988;32:219–238.
17.Carvill M: Bitemporal contraction of the fields of vision in pregnancy. Am J Ophthalmol 1923;6:885–891.
18.Finlay CE: Bitemporal contraction of visual fields in pregnancy. Arch Ophthalmol 1923;52:50–55.
19.Miller NR, Newman NJ: Walsh and Hoyt’s Clinical Neuro-Ophthalmology, Vol. 3, 5th Ed. Baltimore: Williams & Wilkins, 1998;1467–1468.
20.Kass MA, Sears ML: Hormonal regulation of intraocular pressure. Surv Ophthalmol 1977;22:153–176.
21.Qureshi IA: Intraocular pressure: association with menstrual cycle, pregnancy, and menopause in apparently healthy women. Chin J Physiol 1995;38(4):229–234.
22.Horven I, Gzonnaess H: Corneal indentation pulse and intraocular pressure in pregnancy. Arch Ophthalmol 1974;91:92–98.
23.Wilke K: Episcleral venous pressure and pregnancy. Acta Ophthalmol 1975;125:40–45.
24.Horven I, Gjonnaess H, Kroese A: Blood circulation changes in the eye and limbs with relation to pregnancy and female sex hormones. Acta Ophthalmol 1976;54:203–207.
25.Patterson G, Miller SJ: Hormonal influence in simple glaucoma. A preliminary report. Br J Ophthalmol 1963;47:129–137.
26.Posthumus RG: The use and the possibilities of progesterone in the treatment of glaucoma. Ophthalmologica 1952;124:17–25.
27.Meyer EJ, Leibowitz H, Christman EH, et al: Influence of norethynodrel with mestranol on intraocular pressure in glaucoma. Arch Ophthalmol 1965;75:157–161.
28.Sears ML, Mead A: A major pathway for the regulation of intraocular pressure. Int Ophthalmol Clin 1983;6:201–212.
29.Imre J: Pregnancy and the eye, their endocrinological relations. XV Concilium Ophthalmol Egypte 1937;3:213–226.
30.Brent RL: Editorial comment on “Teratogen update: Bendectin.” Teratology 1985;31:429–431.
31.Kooner KS, Zimmerman TJ: Antiglaucoma therapy during pregnancy—part I. Ann Ophthalmol 1988;20:166–169.
32.Shepard TH: Human teratogenicity. Adv Pediatr 1986;33:225–268.
33.Reece AA, Hobbins JC, Mahoney MJ, et al: Medicine of the Fetus and Mother, 2nd Ed. Philadelphia: JB Lippincott, 1992;327–346.
532 Management of Glaucoma in Pregnancy
34.Flach AJ: Glaucoma treatment and pregnancy (correspondence). Arch Ophthalmol 1991;109:463.
35.Mitchell AA: Drugs and birth defects. Clin Toxicol Rev 1982;4(10):1–2.
36.Miller RK: Drugs during pregnancy: a therapeutic dilemma. Rational Drug Ther 1981; 15(7):1–9.
37.Zimmerman TJ, Kooner KS, Kandarakis AS, et al: Improving the therapeutic index of topically applied ocular drugs. Arch Ophthalmol 1984;102:551–553.
38.Kooner KS, Zimmerman TJ: Antiglaucoma therapy during pregnancy—part II. Ann Ophthalmol 1988;20:208–211.
39.Spaeth GL: Glaucoma treatment and pregnancy. Arch Ophthalmol 1990;108:1536.
40.Riddiough MA: Preventing, detecting, and managing adverse reactions of antihypertensive agents in the ambulant patient with hypertension. Am J Hosp Pharm 1977;34:465.
41.Rayburn WF, Zuspan FP: Drug Therapy in Obstetrics and Gynecology, 3d Ed. St. Louis: Mosby Year Book, 1992;194–197.
42.Butters L, Kennedy S, Rubin PC: Atenolol in essential hypertension during pregnancy. Br J Med 1990;301:587–589.
43.Schocken DD, Caron MG, Lefkowitz RJ: The human placenta. A rich source of beta-adrenergic
receptors: characterization of the receptors in particulate and solubilized preparations. J Clin Endocrinol Metab 1980;50:1082–1088.
44.Whitsett JA, Johnson CL, Noguchi A, et al: Beta-adrenergic receptors and catacholamines sensitive adenylate cyclase of the human placenta. J Clin Endocrinol Metab 1980;50:27–32.
45.Schocken DD: Adrenergic receptors of the placenta. Trends Pharmacol Sci 1982;3:215–217.
46.Barnett DB, Cook N, Nahorski SR: Heterogeneity of -adrenoreceptor subtypes in the human placenta. J Auton Pharmacol 1982;2:103–110.
47.Falkay G, Kovacs L: Beta-adrenergic receptors in early human placenta: characterization of [3H]-dihydroalprenolol binding. Life Sci 1983;32:1583–1590.
48.Schneider H, Proegler M: Placental transfer of beta-adrenergic antagonists studied in an in vitro perfusion system of human placental tissue. Am J Obstet Gynecol 1988;159(1):42–47.
49.Cottle MK, Van Petten GR, van Muyden P: Maternal and fetal cardiovascular indices during fetal hypoxia due to cord compression in chronically cannulated sheep. I. Response to timolol. Am J Obstet Gynecol 1983;146:678–685.
50.Blaul G: [Local beta blockaders in pregnancy]. Klin Monatsbl Augenheilk 1985;187:57–59.
51.Fishman WH, Chesner M: Beta-adrenergic blockers in pregnancy. Am Heart J 1988;115:147.
52.Morselli PL, Boutroy MJ, Bianchetti G, et al: Placental transfer and perinatal pharmacokinetics of betaxolol. Eur J Clin Pharmacol 1990;38:477–483.
53.Boutroy MJ, Morselli PL, Bianchetti G, et al: Betaxolol: a pilot study of its pharmacological and therapeutic properties in pregnancy. Eur J Clin Pharmacol 1990;38:535–539.
54.Lustgarten JS, Podos SM: Topical timolol and the nursing mother. Arch Ophthalmol 1983;101:1381–1382.
55.Samples JR, Meyer SM: Use of ophthalmic medications in pregnant and nursing women. Am J Ophthalmol 1988;106(5):616–623.
56.Woods DL, Morrell DF: Atenolol: side effects in a newborn infant. Br Med J 1982;285: 691–692.
57.Dumez Y, Tchobroutsky C, Hornych H, et al: Neonatal effects of maternal administration of acebutolol. Br Med J (Clin Res Ed) 1981;283:1077–1079.
58.Fox RE, Marx C, Stark AR: Neonatal effects of maternal nadolol therapy. Am J Obstet Gynecol 1985;152(8):1045–1046.
59.Kuzelova M, Jurinova J, Jencova D, et al: [Development of a withdrawal syndrome in a neonate after long-term therapy of a mother with metipranolol during pregnancy]. Cesk Pediatr 1993;48:608–610.
60.Fidler J, Smith V, De Swiet M: Excretion of oxprenolol and timolol in breast milk. Br J Obstet Gynaecol 1983;90(10):961–965.
61.Williams T, Ginther WH: Hazard of ophthalmic timolol. N Engl J Med 1982;306:1485–1486.
62.Burnstine RA, Felton JL, Ginther WH: Cardiorespiratory reaction to timolol maleate in a pediatric patient: a case report. Ann Ophthalmol 1982;14(10):905–906.
63.Committee on Drugs: The transfer of drugs and other chemicals into human milk. Pediatrics 1994;93(1):137–150.
64.Birks A, Prior VJ, Silk E: Echothiophate iodide treatment of glaucoma in pregnancy. Arch Ophthalmol 1968;79:283–285.
65.King RG, Gude NM, Krishna BR, et al: Human placental acetylcholine. Reprod Fertil Dev 1991;3(4):405–411.
66.Sastry BV: Human placental cholinergic system. Biochem Pharmacol 1997;53(11):1577–1586.
67.Landauer W: The teratogenic activity of pilocarpine, pilocarpidine and their isomers, with special reference to the importance of steric configuration. J Exp Zool 1956;132:39–50.
68.Kropp BN, Forward RB: The effect of pilocarpine on teeth and salivary glands in the rat embryo. Anat Rec 1963;145:250–257.
B. Sullivan |
533 |
69.Meiniel R: Neuromuscular blocking agents and axial teratogenesis in the avian embryo. Can axial morphogenetic disorders be explained by pharmacologic action upon muscle tissue? Teratology 1981;23:259–271.
70.Chew EY, Trope GE, Mitchell BJ: Diurnal intraocular pressure in young adults with central retinal vein occlusion. Ophthalmology 1987;94:1545–1549.
71.Morgan CD, Sandler M, Panigel M: Placental transfer of catacholamines in vitro and in vivo. Am J Obstet Gynecol 1972;112:1068–1075.
72.Rosenfeld CR, Barton MD, Meschia G: Effects of epinephrine on distribution of blood flow in the pregnant ewe. Am J Obstet Gynecol 1976;124:156–163.
73.Clapp JF: Effect of epinephrine infusion on maternal and uterine oxygen uptake in the pregnant ewe. Am J Obstet Gynecol 1979;133:208–212.
74.Adamsons K, Mueller-Heubach E, Myers RE: Production of fetal asphyxia in the rhesus monkey by administration of catacholamines to the mother. Am J Obstet Gynecol 1971;109:248–262.
75.Product Information. Propine. Allergan, 1999. Irvine, CA.
76.Product Information. Alphagan. Allergan, 1999. Irvine, CA.
77.Gardey-Levassort C, Ventura MA, Thiroux G, et al: An attempt to identify -adrenoceptors in the human placenta. Dev Pharmacol Ther 1984;7(suppl 1):85–88.
78.Lien EL, Morrison A, Kassarich J, et al: Alpha-2-adrenergic control of prolactin release. Neuroendocrinology 1986;44(2):184–189.
79.Product Information. Iopidine. Alcon Laboratories, 1999. Fort Worth, TX.
80.Schardein JL: Chemically Induced Birth Defects, 2d Ed. New York and Basel: Marcel Dekker, 1993;82–85.
81.Wilson JG, Maren TH, Takano K, et al: Teratogenic action of carbonic anhydrase inhibitors in the rat. Teratology 1968;1:51–60.
82.Holmes LB, Kawanishi H, Munoz A: Acetazolamide: maternal toxicity, pattern of malformations, and litter effect. Teratology 1988;37:195–202.
83.Scott WJ, Hirsh KS, DeSesso JM, et al: Comparative studies on acetazolamide teratogenesis in pregnant rats, rabbits, and rhesus monkeys. Teratology 1981;24:37–42.
84.Landauer W, Wakasugi NL: Teratological studies with sulfonamides. J Embryol Exp Morphol 1968;20:261–284.
85.Worsham GF, Beckman EN, Mitchell EH: Sacrococcygeal teratoma in a neonate. Association with maternal use of acetazolamide. JAMA 1978;240(3):251–252.
86.McBride WG: The teratogenic action of drugs. Med J Aust 1963;2:689–693.
87.Heinonen OP, Slone D, Shapiro S: Birth Defects and Drugs in Pregnancy. Littleton, MA: Publishing Sciences Group, 1977;372.
88.Dieckmann WJ, Harrod J, Monardo A: The treatment of preeclamptic edema with acetazolamide (Diamox). Am J Obstet Gynecol 1957;73:789–804.
89.Merlob P, Litwin A, Mor N: Possible association between acetazolamide administration during pregnancy and metabolic disorders in the newborn. Eur J Obstet Gynecol Reprod Biol 1990;35:85–88.
90.Crane CH: Effect on fetus of mother taking a diuretic. JAMA 1957;165:1517.
91.Soderman P, Hartvig P, Fagerlund, C: Acetazolamide excretion into human breast milk. Br J Clin Pharmacol 1984;17(5):599–600.
92.Product Information. Azopt. Alcon Laboratories, 1999. Fort Worth, TX.
93.Product Information. Trusopt. Merck, 1999. West Point, PA.
94.Sciarra JJ: Gynecology and Obstetrics, Vol. 5, Rev. Ed. Philadelphia: Lippincott-Raven. 1998;41–43.
95.Product Information. Xalatan. Pharmacia & Upjohn, 1999. Kalamazoo, MI.
96.Persaud TV: The effects of prostaglandin F2(alpha) on pregnancy and fetal development in mice. Toxicology 1974;2:25–29.
97.Matsuoka Y, Fujita T, Nozato T, et al: Toxicity and teratogenicity of prostaglandin F2 alpha. Iyakuhin Kenkyu 1971;2:403–413.
98.Chang MC, Hunt DM: Effect of prostaglandin F2 alpha on the early pregnancy of rabbits. Nature 1972;236:120–121.
99.Hilbelink DR, Chen LT, Lanning JC, et al: Pregnancy and fetal development in hamsters treated with prostaglandin F2(alpha). Prostaglandins Leukotrienes Med 1982;8:399–402.
100.Karim SM: Physiological role of prostaglandins in the control of parturation and menstruation. J Reprod Fertil Suppl 1972;16:105.
101.Sideris EB, Yokochi K, Coceani F, et al: Prostaglandins and fetal cardiac output distribution in the lamb. Am J Physiol 1985;248:853–858.
102.Printz MP, Skidgel RA, Friedman WF: Studies of pulmonary prostaglandin biosynthetic and catabolic enzymes as factors in ductus arteriosus patency and closure. Evidence for a shift in products with gestational age. Pediatr Res 1984;18:19–24.
103.Philips JB, Lyrene RK: Prostaglandins, related compounds, and the perinatal pulmonary circulation. Clin Perinatol 1984;11:565–579.
534 Management of Glaucoma in Pregnancy
104.Craft IL, Musa BD: Hypertonic solutions to induce abortion. Br Med J 1971;2(752):49.
105.Petter C: Lesions des extremities provoquees chez le foetus de rat par des injections intraveineuses de mannitol hypertonique a la mere. CR Soc Biol 1967;161:1010–1014.
106.Ross MG, Leake RD, Ervin MG, et al: Fetal lung fluid response to maternal hyperosmolality. Pediatr Pulmonol 1986;2:40–43.
107.Ross MG, Ervin MG, Leake RD, et al: Bulk flow of amniotic fluid water in response to maternal osmotic challenge. Am J Obstet Gynecol 1983;147:697–701.
108.Lasuncion MA, Lorenzo J, Palacin M, et al: Maternal factors modulating nutrient transfer to fetus. Biol Neonate 1987;51:86–93.
109.Stolp W, Kamin W, Liedtke M, et al: [Eye diseases and control of labor. Studies of changes in the eye in labor exemplified by subconjunctival hemorrhage (hyposphagmas)]. Geburtshilfe Frauenheilk 1989;49(4):357–362.
110.Watson PG, Grierson I: The place of trabeculectomy in the treatment of glaucoma. Ophthalmology 1981;88:175–196.
111.Jay JL, Murray SB: Early trabeculectomy versus conventional management in primary open angle glaucoma. Br J Ophthalmol 1988;72:881–889.
112.Sherwood MB, Migdal CS, Hitchings RA: Initial treatment of glaucoma: surgery or medications. Filtration surgery. Surv Ophthalmol 1993;37:293–299.
113.Migdal CS, Gregory W, Hitchings R: Long-term functional outcome after early surgery compared with laser and medicine in open-angle glaucoma. Ophthalmology 1994;101(10): 1651–1656.
22
Management of Blind,
Painful Eye from Glaucoma
Kamel M. Itani
Definition
How Is Blind, Painful Eye from Glaucoma Defined?
A blind, painful eye is defined as an eye that has no potential for any useful vision. The blindness is primarily due to glaucoma, although there could be associated ocular conditions, namely, retinal detachment, vascular occlusion, intraocular inflammation,1 intraocular hemorrhage, previous ocular surgery, and tumors. Both primary and secondary forms of glaucoma may be encountered. The loss of vision is absolute, with minimal or no light perception, though certain patients have vision of hand movements. Other causes of pain are ruled out, such as corneal ulcers, corneal abrasions, scleritis, and infected scleral buckles.2
What Is the Etiology of Blind, Painful Eye from Glaucoma?
Almost all nerve terminals originating from the somatosensory receptors in the eye gather into the sensory root of the trigeminal nerve.3 Both the short and long ciliary nerves arise from the nasociliary branch of the trigeminal nerve and supply the iris, sclera, trabecular area, ciliary body, and choroid. The iris is particularly densely supplied. The ciliary body also receives a plexus of fibers from the region of the scleral spur. Most of the sensory fibers are distributed in the anterior segment of the ciliary body.3 Presumably, an elevated intraocular pressure (IOP) would affect these nerve endings, leading to significant ocular pain. The level of IOP does not always correspond with the degree of pain. The rate
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536 Management of Blind, Painful Eye from Glaucoma
at which the IOP has increased plays a major role. A sudden sustained increase in IOP even to moderate levels may cause significant intraocular pain.4 On the other hand, marked elevation in the IOP may not be associated with significant pain, if the pressure increase has been gradual. Presumably, the eye adjusts itself to the situation and remains comfortable.4 The pain due to the rapid and persistent rise in IOP is described as a severe ache in the eye or the brow, or only as a severe headache.
A second cause of pain may be from varying degrees of intraocular inflammation, which may be secondary to intraocular vascular engorgement, with associated leakage of proteins and cells. The inflammation in the iris and the accompanying ciliary body spasm lead to pain that is referred and seems to radiate over a larger area served by the trigeminal nerve.5 Intraocular inflammation usually accompanies secondary glaucomas, following vascular occlusion, retinal detachment, and uveitis. The degree of ciliary spasm does not necessarily correlate with the degree of intraocular inflammation, and younger patients tend to have more severe ciliary body spasm than older ones. A third cause of pain in blind glaucomatous eyes may be secondary to the surface abnormalities that may accompany such disorders. The most common are microcystic edema, bullae formation, and epithelial erosions secondary to corneal decompensation from increased IOP. Lastly, some patients may complain of pain after dellen formation, which may occur close to high filtering blebs or other lesions that may interfere with tear dynamics.
Epidemiology and Importance
How Common Is Blind, Painful Eye from Glaucoma?
Glaucoma is a significant cause of blindness in both the developing and the developed worlds.6,7 It accounts for 7.5% of blindness in countries with established market economies, 8% in Latin America and the Caribbean, 12% in Africa and India, and up to 22.7% in China.8 Studies by the World Health Organization suggest that the problem is greater than previously thought.8 Most likely, glaucomatous blindness will continue to increase globally, reflecting aging populations and lack of sufficient eye care resources in poor countries.8 Glaucoma was implicated in 6% of bilateral blindness in one study from Stockholm, Sweden. There are no available data on the incidence of unilateral blindness from glaucoma, though it may be significantly more than the above numbers suggest.
Are There Any Risk Factors Associated with Blind,
Painful Eye from Glaucoma?
The risk factors are similar to those implicated in severe glaucoma. Generally, blindness from glaucoma in the elderly tends to be associated with primary open-angle glaucoma (POAG) and associated complications.9 In this age group, blindness is slowly progressive, and usually painless. Conversely, blindness in younger patients results from acute secondary glaucoma, and is associated with a higher degree of inflammation. It is well recognized that blacks and Hispanics tend to develop a more severe form of glaucoma at a younger age.10–12
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Secondary glaucomas may be at a higher risk of producing pain, because of the tendency to cause a more rapid increase in IOP than POAG. Closed-angle glaucoma and chronic angle-closure glaucoma can induce blindness, which may also be associated with significant intraocular pain.
Diagnosis and Differential Diagnosis
How Is Blind, Painful Eye from Glaucoma Diagnosed?
The degree of visual loss is severe and irreversible. The ocular examination should include visual acuity, which is usually light perception or no light perception (Fig. 22–1). IOP is usually high, although moderate IOPs could be associated with significant pain. Slit-lamp examination may show conjunctival hyperemia, corneal surface irregularities, corneal bullae, stromal edema, corneal opacification, corneal thinning, and keratic precipitates. The anterior chamber could be normal in depth. It can also be shallow, secondary to peripheral anterior synechiae, pupillary block, posterior synechiae with iris bombé, large lens, and intraocular tumors. The iris may be normal in appearance; however, iris atrophy, neovascularization, and vascular engorgement may be present. The pupil could be fixed and nonreactive to light stimulation. Such eyes may be phakic with normal lenses, but cataract is very common. Pseudophakia is also not uncommon. The vitreous may be hemorrhagic, or it could contain cellular inflammatory debris and membrane formation. A retinal detachment may be present. If the fundus cannot be visualized, then a B-scan echography should be performed to rule out intraocular tumors.13–16 The tumors in such eyes are usually not detected early and tend to grow to significant size, and hence are more likely to produce pain, either secondary to the inflammation, or elevated IOP. Treatable causes of intraocular inflammation should be ruled out, such as sarcoidosis, sympathetic ophthalmia, human leukocyte antigen (HLA)- related uveitis, and autoimmune diseases. Also, exclude other causes of ocular pain, such as scleritis, corneal ulcers, infected scleral buckles, and orbital inflammatory diseases.
Treatment and Management
How Is Blind, Painful Eye from Glaucoma Managed?
The treatment of a blind eye secondary to glaucoma depends on the degree of blindness and pain. This chapter focuses on those eyes with no useful vision and that are painful (Fig. 22–1). Some of these eyes may have undergone one or more surgical procedures, some of which could be for the control of glaucoma. Others may have had no previous surgical intervention. A significant number of eyes, blind from glaucoma, are cosmetically acceptable, while some may be phthisical, irritable, and cosmetically unacceptable. Treatment of blind glaucomatous eyes should be directed toward the comfort of the patient and cosmetic appearance. It should not be directed toward a specific IOP reading. In fact, some patients may have a very high IOP, but with a normal-appearing, comfortable eye. Others may have lower IOP with significant irritation, pain, and poor cosmesis. The treatment is oriented toward three distinctively different groups.
538 Management of Blind, Painful Eye from Glaucoma
Figure 22–1. Management of a patient with blind, painful eye from glaucoma.
The first group has a normal-appearing globe with or without redness. This group can sometimes be satisfactorily treated by lowering the IOP by a few millimeters of mercury. One should avoid long-term carbonic anhydrase inhibitors, because of the systemic side effects.17–19 It may also be wise to avoid using more than two or three topical medications because of side effects, cost,
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and noncompliance. If the pain and the irritation are not controlled, an alternative treatment should be considered. One should also avoid the use of habitforming analgesics.
The second group of glaucomatous blind eyes is characterized by intraocular inflammation, which may be secondary to extensive rubeosis irides, resulting from a variety of causes, such as vascular occlusions, previous surgeries, and tumors. This group can be treated with cycloplegic agents, typically atropine, and antiinflammatory agents, such as steroids or nonsteroidal antiinflammatory drugs. The cycloplegics help decrease the pain associated with ciliary spasm. The steroids help control the inflammation. Care should be taken to watch for secondary bacterial, fungal, and viral infections, especially herpes simplex outbreaks. One or two topical glaucoma medications may also be used. Cholinergic agents such as pilocarpine should be avoided because of their effect on the blood–aqueous barrier and ciliary spasm. The prostaglandin analogue latanoprost (Xalatan) may also increase intraocular inflammation.20,21
The third group of glaucomatous blind eyes is characterized by surface irritation, whether due to bullous corneal disease or calcification. These patients may present as an isolated entity or be part of the above-mentioned two groups.
When managing patients with blind, painful eyes, one should always keep in mind the patient as a whole. The majority of such patients are distressed, uncomfortable, and lead miserable lives. The preoccupation with their eyes overshadows other aspects of their lives and could lead to severe personal, emotional, and economic problems. If the pain is severe, they may not be able to carry on normal lives, and may thus lose their jobs. Another factor to consider is the increased frequency of their office visits. Because of the blindness, these patients do not drive, and hence depend on other family members for transportation. Thus, these visits are inconvenient; they are also costly. It is prudent to discuss these problems with the patient and family. Various treatment modalities and their risks and benefits should be mentioned. Management should be directed toward as quick a recovery as possible.
What Is the Medical Treatment?
Medical treatment should be safe, simple, and effective. If the pain is secondary to high IOP, a mild to moderate decrease in the pressure may resolve the pain. The objective here is not to maximally decrease the IOP, but to reduce it to an acceptable level. Such a decrease in IOP may be achieved by one or two topical medications, preferably with once or twice daily doses. If possible, one should avoid topical medications that require frequent instillation. Similarly, longterm use of systemic medications should be discouraged. Systemic carbonic anhydrase inhibitors tend to have more side effects and should not be part of a long-term treatment. Typically, a beta-blocker, prostaglandin analogue, α-2 adrenergic agonist, or topical carbonic anhydrase inhibitors is the preferred medication. If the pain is secondary to intraocular inflammation, then a cycloplegic agent, preferably atropine, is necessary to control the ciliary body spasm, and obtain relief from pain. Topical steroids are used to control the inflammation. Patients should be informed of the potential of secondary bacterial, fungal, and viral infections. Systemic steroids should be avoided. If the