Ординатура / Офтальмология / Английские материалы / Clinical Pathways in Glaucoma_Zimmerman, Kooner_2001
.pdf
540 Management of Blind, Painful Eye from Glaucoma
pain is secondary to a surface disease, then frequent corneal lubrication should be the treatment of choice. If a band keratopathy is present, one may consider chelation, although more aggressive surgical treatment may be appropriate.
Does Cyclocryotherapy Work?
Freezing of the ciliary body as a treatment of increased IOP has been well studied and extensively reported in the literature.22–23 It can be used in refractory cases. The preferred approach is to treat 180 degrees of the ciliary body at a time. Most surgeons prefer a double freeze-thaw technique. The usual parameters are 80°C for 1 minute. The treatment consists of applying the cryoprobe 2 to 3 mm posterior to the limbus so as to create an iceball that just overlies the limbus. The aim is to cause the least amount of damage to functional trabecular meshwork. It is important to avoid the 3 and 9 o’clock positions, so that the two long posterior ciliary arteries are not damaged. About four or five partially overlapping cryoburns are usually sufficient. Cyclocryotherapy is highly efficacious and may be repeated if the result is unsatisfactory. Complications include persistent hypotony with extensive atrophy of the ciliary body, and the eye may end up as phthisis bulbi. Cyclocryotherapy may also prolong or induce intraocular inflammation. There have been a few cases reported in the literature of sympathetic ophthalmia, which could be devastating to the fellow eye, and hence, the patient should be warned of this potential complication.24,25
Does Laser Cyclodestruction Work?
Neodymium:yttrium-alumninum-garnet (Nd:YAG) laser has been reported as a treatment of high IOP, both in seeing and nonseeing eyes.26–28 Al-Ghamdi et al29 treated 47 patients with Nd:YAG laser, with the mean IOP dropping from 40.5 to 15.6 mm Hg. The treatment was performed after retrobulbar anesthesia, by applying laser burns 2 to 3 mm posterior to the limbus. A mean of 28 burns were applied with an average energy of 6 joules. Complications included intraocular inflammation, hypopyon, hyphema, hypotony, choroidal detachment, and flat anterior chamber.
When Should Retrobulbar Neurolytic Agents Be Used?
For a long time retrobulbar alcohol injection was the treatment of choice in blind painful eyes because of the simplicity of its delivery and apparent effectiveness.30 Over the years, more and more potential severe complications were described, which made the procedure less popular. Complications include ptosis and external ophthalmoplegia. Recurrence of the pain is very common, necessitating repeated alcohol injections. Its effect on the orbital tissues is also of concern. Newer neurolytic agents commonly used in pain management have not been tried in the retrobulbar area.
What Is the Surgical Treatment of Blind, Painful Eye from Glaucoma?
In the absence of visual potential, intraocular glaucoma surgery is contraindicated, because of the risk of sympathetic ophthalmia.31 It should also be
K. Itani |
541 |
avoided because of postoperative complications, and the requirement for intensive follow-up care and a vigorous medication schedule. Any other planned surgical treatment must result in complete cessation of pain and provide good cosmesis. Most patients by this stage have had a long-standing loss of vision and significant pain or poor cosmesis. They usually request that their eye be removed. They have to be educated about the different procedures available. It should also be stressed that once such procedures are performed, there is complete irreversible loss, not only of vision, but also of the eye. However, they should be comforted about the effectiveness of this treatment. The patient and family need to be assured that such a procedure should control the pain and result in good cosmesis. Showing pictures of patients with prosthetic eyes is highly effective in decreasing the anxiety of patients regarding the postoperative cosmesis. Following removal of an eye, patients undergo a grief reaction with the characteristic denial followed by depression or anger and then acceptance and rehabilitation.31
What Is Evisceration?
Evisceration is a surgical procedure in which the intraocular contents are evacuated after the corneal tissue has been removed. The extraocular muscles are not disturbed, and the patient’s own sclera acts as the wrapping around the orbital implant.32,33
What Is Enucleation?
Enucleation is a surgical procedure in which the eye is removed in total and intact. That includes the cornea, the sclera, and the intraocular contents. The extraocular muscles are preserved and some are attached to the orbital implant.32,34
What Are the Advantages and Disadvantages of
Evisceration and Enucleation in the Management of
Blind, Painful Eye from Glaucoma?
The literature is rich with cases of sympathetic ophthalmia following evisceration.35,36 Because of this risk, the procedure of choice for a long time has been enucleation.37 Reports in the literature dispute any significant risk of sympathetic ophthalmia.38–40 Many surgeons perform evisceration if an intraocular tumor can be ruled out. Evisceration has some advantages over enucleation, namely limited changes in orbital anatomy and physiology.32,33 Enucleations induce multiple changes in orbital anatomy and physiology, such as fat atrophy, decreased orbital soft tissue volume, changes in the levator muscle, and decreased orbital blood flow.32 Eviscerations tend to have a better motility because the extraocular muscles are not disturbed. In enucleations, most surgeons would not reattach the oblique muscles, which leads to lesser motility as compared to eviscerations. Eviscerations are technically easier and are usually simpler and faster to perform. Compared to enucleations, there is limited perioperative morbidity and immediate and late operative complications. Enucleations, on the other hand, essentially eliminate the risk of sympathetic
542 Management of Blind, Painful Eye from Glaucoma
ophthalmia and are safer in cases of occult or missed intraocular tumors. They also provide better specimens for pathologic examination, which in some cases may reveal important information concerning the pathogenesis of the visual loss in a variety of ocular disorders. Both procedures are generally performed under general anesthesia, but both could be performed under retrobulbar anesthesia, although it is more challenging with enucleations.
What Is the Surgical Technique in Evisceration?
After retrobulbar or general anesthesia, a 360-degree peritomy is performed and dissection in the sub-Tenon’s space is carried out for 3 to 4 mm posterior to the limbus. With a no. 11 blade, a stab incision just posterior to the limbus is made. The cornea with a small rim of sclera is then resected with scissors. An evisceration spoon is then introduced between the uveal tissue and the sclera, and pushed gently posteriorly in the suprachoroidal space. Blunt dissection with the spoon is then carried over 360 degrees, releasing any adhesions between the choroid and the sclera. At this point, the intraocular contents usually present as an intact mass and are carefully evacuated. The specimen is then sent for pathologic examination. Any bleeding can be controlled with simple pressure. The inside of the sclera is then inspected for any residual uveal tissue. It is advisable to strip any remaining uvea from the sclera to minimize any stimulus for sympathetic ophthalmia. Once the sclera is void of uveal tissues, many surgeons introduce cotton wedges soaked with absolute alcohol and gently but thoroughly scrub the inside of the sclera. This may further decrease the possibility of sympathetic ophthalmia, by destroying any uveal tissues that may still remain in the scleral emissura. Care should be taken to prevent any contact of the alcohol with the conjunctiva because of the possibility of significant postoperative chemosis.
An appropriately sized sphere can then be inserted into the scleral pouch and the sclera sutured with multiple interrupted permanent sutures. The size of such a sphere in eviscerations is usually smaller than desired for optimal orbital volume replacement, hence necessitating a larger prosthesis. To be able to put a larger orbital implant, relaxing incisions in the sclera can be made in a vertical fashion starting from anterior to the equator and going all the way posteriorly to just before the optic nerve area.33,35 A circular incision around the optic nerve can be made connecting these vertical incisions. This will cause the scleral pouch to significantly enlarge. A spherical implant of a larger size can then be inserted. Newer implants, such hydroxyapatite or Medpor, have the advantage of allowing vascularization. Hence, they become a living part of the orbit and decrease the potential long-term complications, especially migration of the implant. Tenon’s capsule is then sutured with multiple interrupted 5-0 polypropylene sutures and the conjunctiva closed with a running 6-0 polypropylene suture. A conformer is then placed and a pressure dressing applied. The dressing should not be disturbed for 48 hours. Five weeks following evisceration, a prosthesis may be fitted.
What Is the Surgical Technique for Enucleation?
Enucleations are usually performed under general anesthesia, although retrobulbar anesthesia can be tried in certain patients.41 After a 360-degree
K. Itani |
543 |
peritomy, dissection is carried out in all of the four cardinal quadrants.42–44 Each rectus muscle is then carefully isolated and disinserted from the globe, after securing a 5-0 polypropylene suture close to the insertion. The superior oblique muscle can be identified and cut. Similarly, the inferior oblique muscle can be isolated, cut, and cauterized. The stump of medial rectus muscle is then secured with a clamp, and the enucleation scissors introduced medial to the globe, directing posteriorly between the medial rectus muscle and the sclera, until the optic nerve is felt and engaged. The tips of the scissors should be directed posteriorly, and while applying pressure anteriorly on the medial rectus stump, the optic nerve is excised. This usually causes immediate protrusion of the globe. Any remaining adhesions between the globe and the orbital tissues are then carefully dissected. Immediate pressure is then applied to the orbit, using a sterile test tube wrapped in gauze. The risk of bleeding can be significantly decreased by first clamping the optic nerve before it is cut. In most cases, bleeding is controlled using a combination of pressure, cautery, and Gelfoam soaked with thrombin. An orbital implant, wrapped in donor sclera, is then introduced into the orbit, and each of the four rectus muscles is sutured to the sclera corresponding to its anatomic position. The rectus muscles can also be sutured directly to the orbital implant without a sclera wrap. A hydroxyapatite or a Medpor implant is preferred because of their ability to promote vascularization and thus decreasing the risk of migration. Tenon’s capsule and conjunctiva are then closed in a manner similar to eviscerations. Similarly, a conformer and a pressure dressing are applied.
What Are the Complications of Evisceration and Enucleation?
The most dreaded intraoperative complication is removal of the wrong eye. This can be prevented by identifying and marking the eye to be operated on preoperatively. The mark should be applied above the correct eye and should be visible in the operative field. Hemorrhage is more common following enucleations, and may be profuse. It is best controlled by applying gauze packing and careful firm pressure following the removal of the globe. Cauterization and thrombin application may also be used appropriately. Injury to the medial orbital wall may be prevented by introducing the enucleation scissors medial to the globe rather than temporal. Similarly, perforation of the globe may be avoided by directing the enucleation scissors posteriorly into the orbit and applying anterior pressure on the media rectus stump. If perforation does occur, every attempt should be made to identify the remaining part of the globe and resecting meticulously. Postoperatively, complications include wound dehiscence with extrusion of the orbital implant. This can be avoided by careful closure of the Tenon’s capsule and conjunctiva in separate layers. Implant migration may be minimized by using hydroxyapatite or Medpor implants. Other complications include ptosis, enophthalmos, shallowing of the fornices, superior sulcus deformity, and orbital cysts.45
What Are the Considerations in Children?
The growth of the orbit in children is dependent on the presence of an enlarging globe. A marked increase in the size of the globe from congenital glaucoma
544 Management of Blind, Painful Eye from Glaucoma
leads to a larger bony orbit, and hence facial asymmetry in children. An absence of a globe will remove the stimulus for a normal enlargement of the bony orbit and hence asymmetry in unilateral cases. Normally, the bony orbit achieves almost adult size by the age of 3 years. Children who undergo enucleations or eviscerations should be followed closely by an ophthalmologist and an oculist, especially those younger than 3 years of age, to ensure adequate development of the bony orbit. This could be achieved by progressively increasing the size of the prosthesis and in some cases larger orbital implants may be needed.
Future Considerations
With the improvement in pain management, newer agents may contribute to better control of pain without the need for removal of the eye.
References
1.Rothova A, Suttorp-van Schulten MS, Frits Treffers W, et al: Causes and frequency of blindness in patients with intraocular inflammatory disease. Br J Ophthalmol 1996;80:332–336.
2.Glatt HJ, Miller JH Jr: Prevention of enucleation of two phthisical eyes by removal of extruding silicone scleral buckles [letter]. Am J Ophthalmol 1993;116:645–646.
3.Williamn HR (ed): Adler’s Physiology of the Eye, 9th Ed. St. Louis: Mosby Year Book, 1992;71–78.
4.Epstein D (ed): Chandler and Grant’s glaucoma, 3d ed. Philadelphia: Lea and Febiger, 1986; 4–5.
5.Intraocular inflammation and uveitis. In: Basic and Clinical Science Course. San Francisco: American Academy of Ophthalmology, 1995–96;57.
6.Mansour AM, Kassak K, Chaya M, et al: National survey of blindness and low vision in Lebanon. Br J Ophthalmol 1996;81:905–906.
7.Blomdahl S, Calissendorff BM, Tengroth B, et al: Blindness in glaucoma patients. Acta Ophthal Scand 1997;75:589–591.
8.Thylefors B, Negrel AD, Pararajasegaram R, et al: Global letter of blindness. Bull WHO 1995;73:115–121.
9.Martin MJ, Sommer A, Gold EB. Race and primary open angle glaucoma. Am J Ophthalmol 1985;99:383–397.
10.Leske MC, Troutman HT, Brook S, et al. Glaucoma in Barbados. Arch Ophthalmol 1989; 107:169.
11.Hiller R, Kahn HA. Blindness from glaucoma. Am J Ophthalmol 1975;80:62–69.
12.Wilensky JT, Ghandi N, Pan T. Racial influences in open angle glaucoma. Ann Ophthalmol 1978;10:1398–1402.
13.Ossoinig KC: Standardized echography: basic principles, clinical applications, and results. Int Ophthalmol Clin 1979;19:127–210.
14.Byrne SF: Standardized echography of the eye and orbit. Neuroradiology 1986;28:618–640.
15.Shammus HG: Atlas of Ophthalmic Ultrasonography and Biometry. St. Louis: CV Mosby, 1984;57–100.
16.Green RL, Byrne SF: Diagnostic ophthalmic ultrasound. In: Ryan SJ (ed): Retina, Vol. 1. St. Louis: CV Mosby, 1989;9.
17.Epstein DL, Grant WM: Carbonic anhydrase inhibitor side effects; serum chemical analysis. Arch Ophthalmol 1977 95:1378–1382.
18.Wallace TR, Fraunfelder FT, Petursson GJ, et al: Decreased libido—a side effect of carbonic anhydrase inhibitor. Ann Ophthalmol 1979;11:1563.
19.Fraunfelder FT, Bagby GC: Possible hematologic reactions associated with carbonic anhydrase inhibitors, JAMA 1989;261:2257.
20.Alm A, Stjeinschultz J, the Scandinavian Latanoprost Study Group: Effects on intraocular pressure and side effects of 0.005% latanoprost applied once daily, evening or morning. Ophthalmology 1995;102:1743–1752.
K. Itani |
545 |
21.Drotzman CE, Woodward DF. Prostanoid–induced blood-aqueous barrier breakdown in rabbits involving the EP2 receptor subtype. Invest Ophthalmol Vis Sci 1990;31:2463–2466.
22.Caprioli J, Strang SL, Spaeth GL, et al: Cyclocryotherapy and the treatment of advanced glaucoma. Ophthalmology 1985;92:947–954.
23.Krupin T, Mitchell KB, Becker B: Cyclocryotherapy in neovascular glaucoma. Am J Ophthalmol 1978;86:24–26.
24.Biswas J, Fogla R: Sympathetic ophthalmia following cyclocryotherapy with histopathologic correlation. Ophthalmic Surg Lasers 1996;27:1035–1038.
25.Harrison TJ: Sympathetic ophthalmia after cyclocryotherapy of neovascular glaucoma with ocular penetration. Ophthalmic Surg 1993;24:44–46.
26.Beckman H, Sugar HS: Neodymium laser cyclocoagulation. Arch Ophthalmol 1973;90:27–28.
27.Cyrlin MN, Bechman H, Czedik C: Neodymium YAG laser transscleral cyclocoagulation treatment for severe glaucoma. Invest Ophthalmol Vis Sci Suppl 1985;26:157.
28.Hampton C, Shields MB, Miller KN, et al: Evaluation of a protocol for transscleral neodymium–YAG cyclophotocoagulation in 100 patients. Ophthalmology 1990;97:910–917.
29.AlGhamdi S, Al-Obeidan S, Tomey K, et al: Transscleral neodymium-YAG laser cyclophotocoagulation for end-stage glaucoma, refractory glaucoma, and painful blind eyes. Ophthalmic Surg 1993;24:526–529.
30.Olurin O, Osuutokun O: Complications of retrobulbar alcohol injections. Ann Ophthalmol 1978;10:474–476.
31.Jennings T, Tessler HH: Twenty cases of sympathetic ophthalmia. Br J Ophthalmol 1989;73: 140–145.
32.Chen W: Enucleation, evisceration, and exenteration. In: McCord C, Tannenbaum M, Nunnery W (eds): Oculoplastic Surgery, 3d Ed. New York: Raven Press, 1995;583.
33.Dortzbach R, Woog J: Enucleation, evisceration, or prosthetic fitting over globes. Ophthalmology 1985;92:1249–1255.
34.Kostick D, Limberg J: Evisceration with hydroxyapatite implant. Ophthalmology 1995;102: 1542–1549.
35.Walter WL: Update on enucleation and evisceration surgery. Ophthalmic Plast Reconstruct Surg 1985;1:243–252.
36.Ruedemann AD Jr: Sympathetic ophthalmia after evisceration. Am J Ophthalmol 1964;57: 770–790.
37.Green WR, Maumenee AE, Sanders DE, Smith ME: Sympathetic uveitis following evisceration. Trans Am Acad Ophthalmol Otolaryngol 1972;76:625–644.
38.Levine MR, Pou CR, Lash RH: Is sympathetic ophthalmia a concern in the new millennium? Ophthalmic Plast Reconstruct Surg 1999;15:4–8.
39.Albert DM, Diaz-Roheni R: A historical review of sympathetic ophthalmia and its epidemiology. Surv Ophthalmol 1989;34:1–14.
40.Marad GE. Recent advances in sympathetic ophthalmia. Surv Ophthalmol 1979;24:141–156.
41.Stephenson CM: Evisceration of the eye with expansion sclerotomies. Ophthalmic Plast Reconst Surg 1987;3:249–251.
42.Traquair HM: Local anesthesia in enucleation of the eyeball. Ophthalmic Rev 1916:35:75–89.
43.Callahan MA, Callahan A: Ophthalmic plastic and orbital surgery. Birmingham: Aesculapius, 1979;42–54.
44.Raffo GT: Enucleation and evisceration. In: Duane TD (ed): Clinical Ophthalmology, Vol. 5. Philadelphia: Harper and Row, 1989;1–16.
45.Hornblass A, Bosniak S: Orbital cysts following enucleation: the use of absolute alcohol. Ophthalmic Surg 1981;12:123–126.
This page intentionally left blank
Index
Page numbers followed by f indicate figures. Page numbers followed by t indicate tables.
A
Acanthamoeba, 381
Acetazolamide, 262
acute primary angle-closure glaucoma, 96t administration, 436
hemodialysis, 366 hyphema, 276 lactation, 523t
malignant glaucoma, 251 pregnancy, 526 traumatic glaucoma
sickle cell disease, 369 vs. dorzolamide, 437
Acetylsalicylic acid, 345 Acromegaly, 356
Acute primary angle-closure glaucoma differential diagnosis, 91t gonioscopy, 90t–91t
medical therapy, 96t presentation, 89–91, 90t–91t
Acyclovir, 374, 376 Adenovirus, 378 Adenovirus type 10 kerato-
conjunctivitis, 148 African-Americans, 65
ALT, 459–460
POAG, 31, 59
African sleeping sickness, 380 African trypanosomiasis, 380
diagnosis, 383 incidence, 382 treatment, 384
Age-related macular degeneration (ARMD) angle-closure glaucoma, 234
diagnosis, 234 treatment, 235 Albendazole, 387
Alkylators
uveitis glaucoma, 161 Allopurinol, 384 Alpha-adrenergic agonists
mechanism, 441–442 NTG, 76
types, 441 Alpha-adrenergic antagonists
pigmentary glaucoma, 182 Alpha-adrenergics, 428t
angiotensin-converting enzyme inhibitors, 443
aspirin, 443
calcium channel blockers, 443 diabetes mellitus, 443 diuretics, 443
NSAIDs, 443
thyroid hormone, 443 Alphaclonidine, 45 Alport’s syndrome, 132
ALT. See Argon laser trabeculoplasty Alzheimer’s disease, 392 Aminocaproic acid
hyphema, 276 Aminothiazole hydrochloride
episcleritis
with glaucoma, 151 Amitril, 340 Amitryptiline, 340 Amphetamine, 341 Amyloidosis, 370–372
defined, 370 diagnosis, 371 epidemiology, 370–371 IOP, 370
treatment, 371–372, 371f Anecortave acetate, 346
Angiotensin-converting enzyme (ACE) inhibitors, 434
alpha-adrenergics, 443
carbonic anhydrase inhibitors, 439 miotics, 441
Angle closure elevated IOP
scleritis, 154 scleral buckling, 247
Angle-closure glaucoma, 215 aphakia
treatment, 220 ARMD, 234
post ocular surgery, 258 pseudophakia
treatment, 220 Angle-recession glaucoma, 283–285
defined, 283 diagnosis, 284
differential diagnosis, 284–285 epidemiology, 283–284 mechanism, 283
risk factors, 283–284 trauma, 268 treatment, 285
vs. trabecular injury, 287
547
548 Index
Angles
gonioscopy, 88–89 pediatric examination, 11
Aniridia
glaucoma risks in, 4–5 heredity, 5
Anopheles, 380
Anterior chamber paracentesis traumatic glaucoma
sickle cell disease, 369 Anterior uveitis
with keratitis, 148 Antibiotics, 341–342 Antidepressants, 340 Antiglaucoma agents, 428t
contraindications, 429t Antihistamines, 343 Antiinflammatory agents
blind, painful eye, 539 Antimetabolites, 460, 499–500
uveitis glaucoma, 161 Antioxidants
cataract, 488 Antiparkinsonian agents, 342 Antispasmolytic agents, 342 Aphakia, 214–217
angle-closure glaucoma treatment, 220
defined, 214
differential diagnosis, 215f, 216 epidemiology, 214
open-angle glaucoma, 219 pathogenesis, 214–216, 215f pupillary block, 216 treatment, 217
Apoptosis, 24–25
Apraclonidine, 253
acute primary angle-closure glaucoma, 96t lactation, 523t
laser iridectomy, 99 mechanism, 441 pregnancy, 526 traumatic glaucoma
sickle cell disease, 369 Aqueous humor
conventional outflow, 109 effects on, 110
normal drainage, 109 outflow, 458, 458t production, 458, 458t uveoscleral outflow, 111
Argon laser gonioplasty indications, 98t, 466 Argon laser iridectomy technique, 99, 100t
Argon laser peripheral photocoagulation primary angle-closure glaucoma, 97
Argon laser trabeculoplasty (ALT), 45, 139, 141, 460, 493–495
African-Americans, 459–460 angle recession glaucoma, 285 complications, 464 effectiveness, 464
indications, 462 myopia, 242
pigmentary glaucoma, 182 pregnancy, 529
principles, 462–463 procedure, 463–464 prophylaxis, 463
Artane, 342 Arteriovenous anomalies
raised EVP, 119–123
Arteriovenous malformation (AVMs), 123, 360
Aspirin, 345 alpha-adrenergics, 443 topical beta blockers, 435
Atenolol pregnancy, 524
Atovaquone, 384 Atropine
blind, painful eye, 539 hyphema, 276 malignant glaucoma, 251 uveitis glaucoma, 160
Autoimmune antibodies NTG, 73
Automatic static threshold, 38–39 Autonomic agents, 344 Axenfeld’s syndrome
microcornea with, 3
B
Bacterial endophthalmitis vs. phacoanaphylaxis, 218
Barbiturates, 341
Baylisascaris, 388 Behcet’s disease, 163, 388 Bentyl, 342 Benznidazole, 384
Beta blockers, 45
acute primary angle-closure glaucoma, 96t blood lipid profiles, 435
calcium channel blocker interactions, 434 carbonic anhydrase inhibitors, 439 contraindications, 429t
diabetes mellitus, 435 differences between, 433 HDL, 435
hyphema, 276 IOP, 433 miotics, 441 NTG, 76
pigmentary glaucoma, 181 side effects, 434
systemic with topical, 435
TC/HDL, 435 topical, 434
aspirin, 435
hormone replacement therapy, 435 NSAIDS, 435
thyroid hormone, 435 Birth trauma
cloudy cornea, 14
Blind, painful eye, 535–544 defined, 535
diagnosis, 537 epidemiology, 536–537 etiology, 535–536 evisceration, 541–544 Nd:YAG, 540
POAG, 536–537 prostaglandins, 539 risk factors, 536–537 surgery, 540–544 treatment, 537–544, 538f
Blindness POAG, 34
Blood flow
glaucoma suspects, 63–64 NTG, 72–73
Blood viscosity POAG, 367 Blunt trauma
IOP, 271f–272f, 282f, 289f Bolvidon, 340
Botulinum toxin, 345 Brimonidine, 45, 253, 449
acute primary angle-closure glaucoma, 96t lactation, 523t
laser iridectomy, 99 mechanism, 442 NTG, 76 pregnancy, 526 traumatic glaucoma
sickle cell disease, 369 Brinzolamide
acute primary angle-closure glaucoma, 96t lactation, 523t
pregnancy, 526
vs. dorzolamide, 438 vs. timolol, 436
B-scan ultrasound intraocular tumors, 418
Buphthalmos, 1
Burns. See Thermal injury
C
CAI. See Carbonic anhydrase inhibitors Calcium channel blockers, 448–449 Calcium chelators, 447
Cannabinoids, 446–447 Carbachol, 256
Carbonic anhydrase inhibitors (CAI), 45, 428t
Index 549
acute primary angle-closure glaucoma, 96t angiotensin-converting enzyme inhibitors,
439
beta blockers, 439 blind, painful eye, 538
calcium channel blockers, 438 contraindications, 429t diabetes mellitus, 439 diuretics, 438 hypoglycemics, 439
IOP, 253 mechanism, 436 myopia, 242 NTG, 76
pigmentary glaucoma, 181 pregnancy, 526–527
side effects, 438 types, 436
vs. timolol, 436 Carboplatin, 422 Cardiac glycosides, 434
Cardiogenesis glaucoma, 117
Carotid artery occlusive disease, 230, 360 diagnosis, 231
treatment, 233
Carotid-cavernous sinus fistula (CCSF), 360
raised EVP, 119–120 Carotid-jugular shunts raised EVP, 122–123
Cataracts, 197–200, 255t, 485–509 classification, 198–199, 198t defined, 197–198 demographics, 486
diagnosis, 199–202 differential diagnosis, 200t
epidemiology, 198–199, 485–489 evaluation, 490–491 490t extraction
ghost cell glaucoma, 281 with glaucoma
treatment, 493–507, 494f IOP elevation, 255–256 laser trabeculoplasty, 256 mechanisms, 199t peripheral iridotomy, 257
refractory glaucoma, 502–503 risk, 255
socioeconomic factors, 487 trabeculectomy, 474–475 trauma, 199
traumatic. See Traumatic cataracts. treatment, 256–257
two-stage approach, 499 uncontrolled glaucoma, 497f
Cataract surgery, 503–505
combined with glaucoma surgery, 496t glaucomatous vs. nonglaucomatous eyes,
492–493
