Ординатура / Офтальмология / Учебные материалы / Clinical Diagnosis and Management of ocular trauma

238

Clinical Diagnosis and Management of Ocular Trauma

intraocular inflammation after cataract extraction

miosis during phacoemulsification cataract surgery.

without the risk of a steroidal IOP increase (Herneiss).

Mean horizontal pupillary diameter measurements for

Holzer and associates reported that ketorolac

both medications were similar at the start of surgery.

tromethamine ophthalmic solution 0.5% was is

However, a consistent trend of larger pupillary

effective as loteprednol etabonate ophthalmic

diameter was seen in all subsequent surgical intervals

suspension 0.5% in reducing inflammation after routine

in the ketorolac-treated group. Changes from baseline

phacoemulsi-fication and IOL implantation, suggesting

measurements also indicated a more significant

that ketorolac tromethamine 0.5% is a safe and

inhibition of miosis at all subsequent intervals, and a

effective antiinflammatory alternative to steroids after

more stable mydriasis throughout the procedure in

cataract extraction.

the ketorolac-treated group (Solomon 1997).

Similarly, Solomon and associates reported

ketorolac tromethamine 0.5% is a safe and effective

NSAIDs and Topical Steroids

anti-inflammatory alternative to steroids after cataract

extraction. In that study, ketorolac tromethamine 0.5%

It is well accepted that combination topical therapy

was as effective as rimexolone 1% in reducing

with a corticosteroid and a NSAID is more effective

inflammation after cataract surgery. There were no

than either agent dosed individually for treatment of

between-group differences in signs and symptoms of

CME following cataract surgery, and a recent study

inflammation, intraocular pressure, or Kowa cell and

by Rho and associates supports this paradigm. The

flare measurements in this double-masked, prospective

authors compared combination therapies of diclofenac

evaluation of 36 patients (Solomon and Vroman

sodium 0.1% and prednisolone acetate 1%, with

2001).

ketorolac tromethamine 0.5% and prednisolone

acetate 1%, for treatment of CME in 68 patients

NSAIDs for the Inhibition of

following uncomplicated cataract surgery. Complete

resolution of CME was noted in 28% of diclofenac

Miosis

patients and in 25% of ketorolac patients. Final vision

improved three or more lines in 58% and 53% of

Srinivisin and associates reported that topical ketorolac

patients, respectively. None of the patients showed signs

was a more effective inhibitor of miosis than topical

of corneal toxicity or significant intraocular pressure

diclofenac during extracapsular cataract extraction and

rise during the treatment period. The authors

IOL implantation. Ketorolac also provided a more

concluded that combination therapy with NSAIDs and

stable mydriatic effect throughout surgery. In a study

steroids was effective in reducing the severity of

of 51 patients who were prospectively randomized to

pseudophakic CME and in improving final vision.

receive ketorolac 0.5% or diclofenac 0.1% at 3

The findings of Rho and associates are supported

intervals preoperatively. In this study, the ketorolac

by another recent study by Heier and associates (Heier,

group showed a consistent trend toward larger pupil

2000). That study evaluated the efficacy of ketorolac,

diameters at subsequent surgical intervals as well as

prednisolone acetate 1.0%, and ketorolac and

greater inhibition of miosis in the ketorolac group.

prednisolone combination therapy in the treatment

Similarly, Snyder and associates reported that the

of acute, visually significant, clinical CME following

use of ketorolac as a single agent negated the need

cataract extraction surgery in a randomized, double-

for use of a combination of preoperative NSAID

masked, prospective trial of 28 patients. Treatment was

(flurbiprofen) and postoperative cosrticosteroid for the

continued until CME resolved or for 3 months,

prevention of intraoperative miosis and postoperative

whichever occurred first and then tapered over 3 weeks.

inflammation in cataract surgery. In their study of 26

The average improvements in Snellen visual acuity

patients, there were no statistically significant differences

were 1.6 lines with ketorolac monotherapy, 1.1 lines

in dilation (preoperative versus postoperative) or cell

with steroid monotherapy, and 3.8 lines with

and flare postoperatively. The authors concluded that

combination therapy. More patients in the combination

the use of ketorolac as a single agent could eliminate

group achieved at least a two-line improvement (89%

the expense of using separate anti-inflammatory and

of combination patients versus 67% of ketorolac and

antimiotic preparations preoperatively and post-

50% of steroid patients). Moreover, these patients

operatively, thereby enhancing surgeon convenience

improved faster with combination therapy than with

and patient convenience and compliance (Snyder).

monotherapy with either agent (1.33 months for

Recently, a large study (n=118) compared the

combination therapy compared with 1.43 months for

effects of topical ketorolac with topical 0.03%

ketorolac patients and 2.75 months for steroid

flurbiprofen on the inhibition of surgically induced

patients). Improvements in contrast sensitivity and

Optimizing Visual Outcomes with NSAIDs Therapy in Cataract and Refractive Surgery

239

leakage on fluorescein angiography tended to mirror

concluded that macular edema decreases the quality

improvements in Snellen acuity. The authors concluded

of postoperative vision and that the use of pre-

that treatment of acute, visually significant

operative and postoperative NSAIDs decreases the

pseudophakic CME with ketorolac and prednisolone

amount of postoperative macular edema.

combination therapy appears to offer benefits over

Many clinicians are hesitant to prescribe topical

monotherapy with either agent alone.

NSAIDs for long-term use because of prior reports of

A study by Arshinoff et al evaluated postoperative

corneal melting associated with topical NSAIDs (Flach,

pain in 97 PRK patients using different topical NSAID

Gaynes). However, analysis of NSAID-associated

protocols. In their study, treatment with topical

corneal events implicates the now defunct generic

homatropine hydrobromide, either diclofenac sodium

diclofenac product, diclofenac sodium ophthalmic

or ketorolac tromethamine, and a soft contact lens

solution as the agent primarily responsible (Gaynes).

was most effective in achieving post-PRK analgesia.

The demonstrated safety of ketorolac throughout

They also found that NSAIDs added to topical steroid

numerous studies, some as long as 6 weeks duration,

protocols had a significantly greater effect than steroids

suggests that this drug is safe for extended use. If fact

alone on reducing myopic regression for one year

ketorolac has actually been recommended for the

postoperatively (Arshinoff, 1994).

treatment of post-cataract inflammation in a patient

with systemic steroid treated rheumatoid arthritis post-

phacoemulsification. In this patient the fear of “melting”

Prevention of CME

led the physician to avoid topical NSAIDs. However,

the severe reaction postoperatively led him to using

All available evidence demonstrates that ketorolac is

it successfully in the second eye with excellent results

an effective treatment for acute and chronic CME.

(Caronia).

Several studies, however, suggest that ketorolac is also

The available evidence demonstrates that NSAIDs

able to prevent CME in postoperative patients. A study

are highly effective analgesics for pain associated with

by Flach and associates (1990) suggested that ketorolac

cataract and refractive procedures. The ability to

prevents CME without the risks associated with

provide relief of patient pain is critical because patients

concomitant topical steroid treatment. In that study,

have high expectations and expect almost no pain with

50 patients with bilateral cataracts were enrolled in a

ophthalmic surgeries. Patients who experience ocular

placebo-controlled, paired-comparison, double-

pain or discomfort may therefore believe that their

masked study. Eleven patients had evidence of

surgeon may have substandard surgical skills and the

angiographic (angiographic aphakic CME) ACME on

resulting patient dissatisfaction and potential for

postoperative day 40. Two of these patients demons-

negative word of mouth to the patient’s colleagues

trated bilateral ACME, one patient had ACME in the

and friends may have adverse consequences for a

NSAID-treated eye, and eight patients had ACME in

surgical practice. Choosing the most effective topical

the placebo-treated eye. This was a statistically

agent for relief of ocular inflammation and pain

significant difference favoring drug treatment. In

postoperatively is therefore.

addition, the signs of anterior ocular inflammation were

The adjunctive use of NSAIDs with steroids optimizes

greater in the eyes with ACME.

surgical outcomes as numerous studies have

Roberts presented data from a clinical study at the

demonstrated that the combination of an NSAID and

2005 meeting of ASCRS that demonstrated that

steroid is more effective for the treatment of post-

patients using preoperative and postoperative NSAIDs

operative inflammation, CME, and improving visual

had less postoperative increase in macular thickness

acuity than either NSAID or steroid monotherapy.

than those who did not use NSAIDs. In that study,

Perhaps the most important effect to surgeons is

200 patients undergoing phacoemulsification were

the increased amount of dilation preoperatively and

randomized to two pharmaceutical treatment

the tendency for the dilation to remain for the entire

regimens, differing only by the inclusion/exclusion of

procedure. Some surgeons have likened this effect as

ketorolac 0.4% into the standard treatment regimen.

like having a third hand during surgery. Other studies

Outcome measures included macular thickness by OCT

point out the direct relationship between pupil size and

at preoperative and 4 weeks postoperative, contrast

rate of surgical complications (Donnenfeld).

sensitivity by FACT, and Snellen visual acuity. After 4

In recent years, there has been a substantially

weeks, the change in macular thickness was

amount of debate in the ophthalmic community

substantially greater without NSAIDs than with

regarding the use of NSAIDs prior to surgery to prevent

(10.4 μm compared with 4.2 μm, respectively). There

the formation of CME. We understand and accept that

were no differences in visual acuity. The author

increased inflammation postoperatively is associated

240

Clinical Diagnosis and Management of Ocular Trauma

with an increased risk of developing CME. In fact, a

2.

Caronia RM, Perry HD, Donnenfeld ED, J Cataract and

study by Ursell and associates reported that patients

Refractive Surg 2002;28:1880-81.

who had angiographic CME at day 60 were more likely

3.

Donnenfeld ED, Perry HD, Wittpenn JR, Solomon R,

to have had more postoperative inflammation than

Nattis A, Chou T. Preoperative ketorolac tromethamine

0.4% in phacoemulsification outcomes: pharmacokinetic-

patients who did not develop CME. (Ursell) It follows,

response curve. J Cataract Refract Surg 2006

therefore, that preventing inflammation with pro-

Sep;32(9):1474-82.

phylactic dosing would decrease the risk of developing

4.

Evans RE, Bucci FA Jr, Amico LM. Efficacy of Ketorolac

CME. A recent study by Donnenfeld and associates

0.5% versus Ketorolac 0.4% Following Cataract Surgery.

(Donnenfeld) does provide us with evidence

Presented at ARVO 2005.

supporting the use of ketorolac 0.4% as surgical

5.

Flach AJ, Stegman RC, Graham J, Kruger LP. Prophylaxis

prophylaxis against CME. The study was a prospective

of aphakic cystoid macular edema without corticosteroids.

A paired-comparison, placebo-controlled double-masked

evaluation of 100 patients randomized in a double-

study. Ophthalmology 1990;97:1253-58.

masked fashion prior to phacoemulsification into 4

6.

Flach AJ. Corneal melts associated with topically applied

groups: one group received preoperative ketorolac

nonsteroidal anti-inflammatory drugs. Trans Am

tromethamine 0.4% four times daily for 3 days and

Ophthalmol Soc. 2001;99:205-10; discussion 210-12.

three doses every 15 minutes immediately surgery,

7.

Gaynes BI, Fiscella R. Topical nonsteroidal anti-

another received four doses on the day before surgery

inflammatory drugs for ophthalmic use: a safety review.

ketorolac 0.4% and three doses every 15 minutes

8.

Drug Saf. 2002;25:233-50.

immediately surgery, another received ketorolac only

Goyal R, Shankar J, Fone DL, Hughes DS. Randomized

controlled trial of ketorolac in the management of corneal

3 times (every 15 minutes) in the hour immediately

abrasions. Acta Ophthalmol Scand. 2001 Apr;79(2):

surgery, and the fourth group was randomized to

177-79.

control. In that study, use of ketorolac for 1 or 3 days

9.

Guzek JP, Holm M, Cotter JB, et al. Risk factors for

reduced the incidence of CME. No patients in these

intraoperative complications in 1000 extracapsular

groups had CME at week 2, compared with 12% (3/

cataract cases. Ophthalmology 1987;94:461-66.

25) of control patients and 4% (1/25) of patients in

10.

Heier J, Cheetham JK, Degryse R, et al. Ketorolac

the 1 hour group. This study suggests that three day

tromethamine 0.5% ophthalmic solution in the treatment

of moderate to severe ocular inflammation after cataract

preoperative dosing with ketorolac effectively prevents

surgery: a randomized, vehicle-controlled clinical trial. Am

CME. Other findings of that study demonstrated that

J Ophthalmol 1999;127:253-59.

ketorolac maintained pupil size, reduced discomfort,

11.

Hirneiss C, Neubauer AS, Kampik A, Schonfeld CL.

limited reductions in epithelial cell counts, and reduced

Comparison of prednisolone 1%, rimexolone 1% and

patient need for additional anesthesia. Ketorolac also

ketorolac tromethamine 0.5% after cataract extraction. A

provided substantial reductions in the amount of time

prospective, randomized, double-masked study. Graefes

needed to perform surgery, making it a cost-effective

Arch Clin Exp Ophthalmol 2005 Mar 9; [Epub ahead

of print].

pharmaceutical for cataract surgery. Most of these data

12.

Kaiser PK, Pineda R 2nd. A study of topical nonsteroidal

followed a clear dose-response pattern, suggesting that

anti-inflammatory drops and no pressure patching in the

maximum prophylaxis can be expected with the three

treatment of corneal abrasions. Corneal Abrasion

days dosing regimen, though even 1 day of ketorolac

Patching Study Group. Ophthalmology 1997;104:

was consistently superior to 1 hour of ketorolac or to

1353-59.

control. Flach and Roberts that ketorolac is an effective

13.

McColgin AZ, Heier JS. Control of intraocular

prophylaxis against CME.

inflammation associated with cataract surgery. Curr Opin

Ophthalmol 2000;11(1):3-6.

If a 3-day dosing regimen of ketorolac is effective

14.

Mentes J, Erakgun T, Afrashi F, Kerci G.Incidence of

surgical prophylaxis, what is the most appropriate

cystoid macular edema after uncomplicated

postoperative dosing regimen? In my experience, 4

phacoemulsification. Ophthalmologica 2003 Nov-

weeks of QID dosing with ketorolac 0.4% is optimal

Dec;217(6):408-12.

for most patients, in patients with diabetes mellitus we

15.

O'brien TP. Emerging guidelines for use of NSAID therapy

use at least 6 weeks of therapy and most important

to optimize cataract surgery patient care. Curr Med Res

in patients with diabetic retinopathy we use ketorolac

16.

Opin 2005 Jul;21(7):1131-38.

0.4% for at least three months to help protect this

Polansky JR, Weinreb RN. Steroids as anti-inflammatory

agents. In: Sears ML, ed. Pharmacology of the Eye. New

most susceptible group from developing CME.

York, NY: Springer-Verlag 1984;460-538.

Bibliography

17.

Price FW Jr, Price MO, Zeh W, Dobbins K. Pain reduction

after laser in situ keratomileusis with ketorolac

tromethamine ophthalmic solution 0.5%: a randomized,

1. Arshinoff S, D'Addario D, Sadler C, Bilotta R, Johnson

double-masked, placebo-controlled trial. J Refract Surg.

TM. Use of topical nonsteroidal anti-inflammatory drugs

2002 Mar-Apr;18(2):140-44.

in excimer laser photorefractive keratectomy. J Cataract

18.

Price FW, Tonon E, VanDenburgh AM, Stern K,

Refract Surg. 1994;20:216-22.

Cheetham JK, Schiffman RM. Safety and Efficacy of

Optimizing Visual Outcomes with NSAIDs Therapy in Cataract and Refractive Surgery

241

Reformulated Ketorolac Tromethamine 0.4% Ophthalmic

antimiotic and anti-inflammatory in cataract surgery. J

Solution in Post-Photorefractive Keratectomy Patients.

Cataract Refract Surg 2000;26:1225-27.

Presented at ARVO 2003.

31. Snyder RW, Siekert RW, Schwiegerling J, Donnenfeld E,

19. Price MO, Price FW. Efficacy of topical ketorolac

Thompson P. Acular as a single agent for use as an

tromethamine 0.4% for control of pain or discomfort

antimiotic and anti-inflammatory in cataract surgery. J

associated with cataract surgery. Curr Med Res Opin 2004

Cataract Refract Surg. 2000;26:1225-27.

Dec;20(12):2015-19.

32. Solomon KD, Donnenfeld ED, Raizman M, et al. Safety

20. Quinn CJ. Cystoid macular edema. Optom Clin

and efficacy of ketorolac tromethamine 0.4% ophthalmic

1996;5(1):111-30.

solution in post-photorefractive keratectomy patients. J

21. Ray S. D'Amico DJ. Pseudophakic macular edema.

Cataract Refract Surg. 2004 Aug;30(8):1653-60.

Semin Ophthalmol 2002;17:167-80.

33. Solomon KD, Donnenfeld ED, Raizman M, et al. Safety

22. Rho DS, Soll SM. Combination Therapy for

and efficacy of ketorolac tromethamine 0.4% ophthalmic

Pseudophakic Cystoid Macular Edema: Diclofenac

solution in post-photorefractive keratectomy patients. J

Sodium 0.1% and Prednisolone Acetate 1% Versus

Cataract Refract Surg 2004 Aug;30(8):1653-60.

Ketorolac Tromethamine 0.5% and Prednisolone Acetate

34. Solomon KD, Turkalj JW, Whiteside SB, Stewart JA,

1%. Presented at ARVO 2004.

Apple DJ. Topical 0.5% ketorolac vs 0.03% flurbiprofen

23. Rho DS. Treatment of acute pseudophakic cystoid

for inhibition of miosis during cataract surgery. Arch

macular edema: Diclofenac versus ketorolac. J Cataract

Ophthalmol 1997 Sep;115(9):1119-22.

Refract Surg 2003 Dec;29(12):2378-84.

35. Solomon KD, Turkalj JW, Whiteside SB, Stewart JA,

24. Roberts CW. Comparison of the Ocular Comfort of Acular

Apple DJ. Topical 0.5% ketorolac vs 0.03% flurbiprofen

LS with Acular PF in Healthy Volunteers. Presented at

for inhibition of miosis during cataract surgery. Arch

ARVO 2004.

Ophthalmol 1997;115:1119-22.

25. Roberts CW. Pretreatment with topical diclofenac sodium

36. Solomon KD, Vroman DT, Barker D, Gehlken J.

to decrease postoperative inflammation. Ophthalmology

Comparison of ketorolac tromethamine 0.5% and

1996;103:636-39.

rimexolone 1% to control inflammation after cataract

26. Rossetti L, Autelitano A. Cystoid macular edema

extraction. Prospective randomized double-masked

following cataract surgery. Curr Opin Ophthalmol

study. J Cataract Refract Surg 2001 Aug;27(8):1232-37.

2000;11:65-72.

37. Srinivasan R, Madhavaranga. Topical

ketorolac

27. Sandoval HP, Fernandez de Castro LE, Vroman DT,

tromethamine 0.5% versus diclofenac sodium 0.1% to

Solomon KD.

Comparison

of 0.4%

Ketorolac

inhibit miosis during cataract surgery. J Cataract Refract

Tromethamine Ophthalmic Solution vs 0.5% Ketorolac

Surg 2002 Mar;28(3):517-20.

Tromethamine

Ophthalmic

Solution

to Prevent

38. Stewart R, Grosserode R, Cheetham JK, et al. Efficacy and

Inflammation After Phacoemulsification and Intraocular

safety profile of ketorolac 0.5% ophthalmic solution in

Lens Implantation: A Prospective, Randomized, Double-

the prevention of surgically induced miosis during

Masked, Clinical Trial. Presented at ARVO 2005.

cataract surgery. Clin Ther 1999;21:723-32.

28. Schechter BA, Wittpenn JR. Evaluation of Ketorolac

39. Ursell PG, Spalton DJ, Whitcup SM, Nussenblatt RB.

(Acular LS) During the Induction Phase of Cyclosporine

a (Restasis) Therapy to Improve Patient Comfort.

Cystoid macular edema after phacoemulsification:

Presented at ARVO 2005.

relationship to blood-aqueous barrier damage and visual

29. Singal N, Hopkins J. Pseudophakic cystoid macular

acuity. J Cataract Refract Surg 1999 Nov;25(11):

edema: ketorolac alone vs. ketorolac plus prednisolone.

1492-97.

Can J Ophthalmol. 2004 Apr;39(3):245-50.

40. Waterbury LD, Flach AJ. Efficacy of low concentrations

30. Snyder RW, Siekert RW, Schwiegerling J, Donnenfeld E,

of ketorolac tromethamine in animal models of ocular

Thompson P. Acular as a single agent for use as an

inflammation. J Ocul Pharmacol Ther. 2004;20:345-52.

Management of Cystoid Macular Edema

243

factors like the complement, the platelet activation

of risk factors like cataract surgery, uveitis, posterior

factor, lisozomal enzymes, cytoquines, nitric oxide,

capsulotomy and diabetic retinopathy.

endothelin and interleukin. We can conclude that any

This concepts must be taken in count by the

factor that contributes to the rupture of the barriers

physician at the time to prescribe this medications in

blood-accuous and blood-retinal is going to increase

particular if some risk factors are present in some patient.

the possibility to develope CME.

If the therapy can be done with another medication

it will be better, but if it must be continued for some

MICROVASCULAR DAMAGE

reason, the utilization of non-steroidal

anti-

This is commonly found in diabetic retinopathy,

inflammatory drugs can avoid the development of

CME without loss of the hypotensor effect of the anti-

occlusive diseases like retinal vein occlusions, and other

glaucoma drugs. Also a constant follow-up with the

less commonly diseases like idiopathic juxtafoveal

explanation to the patient of specific symptoms of

capillary telangiectasia. The main factor is again the

macular disease and Amsler test in each visit for

rupture of the intraocular barriers that this vascular

glaucoma control, are mandatory.

alterations produce and the liberation of the mentioned

mediators during the acute vascular event. Some other

PERIPHERAL RETINAL LESIONS

factors like the VEGF and IGF-1 liberated by the

ischemic tissues, have been involved in the rupture

A peripheral lesion, can lead by itself, to the rupture

of the intraocular barriers and so in the production

of the intraocular barriers and so the development of

of CME. Any syndrome associated with sub-retinal

CME. It is a good behavior to explorate the periphery

neovascularization can have the same effect.

of the retina in a case when we find CME and we

are trying to know the cause.

INFLAMMATORY DISEASES

TUMORAL DISEASES

The most well-known form of uveitis that can produce

CME is pars planitis; in fact CME is the main cause

Because of acummulation of leakage and rupture of

of visual loss in this inflammatory process, but many

the barriers, many ocular tumors, like malignant

other forms of uveitis like Behçet´s disease, Crohn´s

melanomas, peripheral capillary hemangiomas and

disease, rheumatoid arthritis, sarcoidosis and some

Coat´s disease can be also cause of CME.

other forms of non-specifical uveitis can produce some

degree of CME. The cause is as mentioned before,

EYE HYPOTONY

the liberation of the inflammatory mediators.

It can be post-traumatic, with or without rupture of

POST-MEDICATION (ANTIGLAUCOMA DRUGS

the globe, it can be followed cataract surgery, glaucoma

procedures or choroidal effussions of any cause. At

AND PRESERVATIVES)

the end, the low intraocular pressure is the cause for

The first reference about the relation between an anti-

the rupture of the intraocular barriers and so the

glaucoma medication and the development of CME

liberation of mediators.

was described by Becker in 1967 and was with the

use of epinephrine; was noted years after, that this

OPTIC NERVE DISEASES

incidence was more in the aphakic patient. It is well

Optic nerve inflammations like true papilledema,

known at this time, that the topical epinephrine

neuropathy or some ischemic diseases can produce

increase the prostaglandins in the eye, in particular

CME.

in the aphakic one, and so the rupture of the

intraocular barriers.

RETINAL TRACTION

Some other medications were described to

produce this effect like dipivalylepinephrine, timolol

Peripheral traction, macular traction, epiretinal

and benzalconium chloride. Recently with the arise of

membranes, and traction produced by diabetic

new pharmacologic groups of anti-glaucomatous

retinopathy (even without direct macular traction) are

medication, in particular prostaglandins, the incidence

common entities that can produce CME.

of post-medication CME has increase. A lot of studies

have been conducted in this field and what we know

FINAL COMMON PATHWAY OF UNDERLYING

currently is that latanoprost, travoprost, bimatoprost

DISEASES

and unoprostone can produce some degree of CME

Ischemic, tractional, inflammatory, toxic and genetic.

and that this incidence can increase with the association

Management of Cystoid Macular Edema

245

of CME because the fluid-filled spaces in the retina

NON-SURGICALAPPROACH

are easily seen. This cross-sectional image of the retina

Many drugs have been involved for the treatment of

can also be helpful in the monitoring over time of the

CME during the time. Some of them are used as a

disease by quantifying the amount of fluid inside the

traditional fashion and some others are emerging as

retina in serial studies. A non-invasive study can be

new therapeutic resources.

the ideal modality in monitoring the response to

treatment.

Nonsteroidal Anti-inflammatory Drugs (NSAIDs)

In particular cases an electroretinogram can also

The main effect of this group of drugs is to estabilize

be helpful but not mandatory (Figs 38.3 to 38.5).

the blood-retinal barrier. This effect is because they

inhibit the enzyme cyclo-oxygenase. They can be used

by systemic way and also in the form of eyedrops.

The main examples of this group of medications are:

1.

Indomethacin

2.

Ketorolac

3.

Diclofenac

They inhibite the prostaglandin synthesis by

decreasing the activity of the enzyme cyclo-oxygenase.

These drugs in the topical form must be used as a

medication in the preoperative and postoperative

period of some intraocular procedures like cataract

Fig. 38.3: Macular quistic edema

surgery, posterior capsulotomy and peripheral

iridectomy for example, to reduce the incidence of

CME. This profilactic form also helps to reduce the

postoperative inflammatory process. As has been said

before, the development of CME in some way

correlates with the degree of manipulation during the

ocular surgery and some factors have been

demonstrated in the development of CME like the

time of light microscope exposure, posterior capsule

rupture and vitreous manipulation. Of course, a real

“clean” surgery can decrease the incidence of CME,

but anyway, the use of NSAIDs

is mandatory. New

operative devices that avoid the use of direct light

Fig. 38.4: CME plus epiretinal membrane

exposure during the ocular surgery are promising in

the near future to decrease the incidence of CME in

uncomplicated surgery cases.

The use of systemic NSAIDs is only reserve for the

cases of complete diagnosis of CME; even so some

surgeons are using them as a profilactic medication.

There is not a recomended time for the use of systemic

NSAIDs for the treatment of CME; the time of use

will depend upon the response of each patient in

particular according the follow-up.

Because sometimes it is a long-term medication,

secondary effects of NSAIDs must be always taken in

count. In the systemic medication, gastric effects should

Fig. 38.5: Epiretinal membrane plus macular cystic edema

be monitoring during the visits of the patient. A history

of gastric diseases including ulcerative disease and

bleeding is mandatory when oral indomethacin is in

Treatment

use. If some of these effects are present the

therapeutic must be suspended and replaced by other

The treatment of CME can be divided in two

medication.

approaches that finally in the practice are combined

Local NSAIDs have also some secondary effects;

but in the theory we are going to describe separately.

long-term use may delay wound healing and has been