reply: pseudophakic pigmentary glaucoma

2
diopter AcrySof MA60 IOL (Alcon Laboratories) in the capsular bag 2 years previously. The man complained of intermittent, painless, blurred vision with intraocu- lar pressure reaching 40 mm Hg and anterior chamber cells, which began a few weeks after bilateral neody- mium:YAG (Nd:YAG) laser capsulotomies. He re- sponded well to atropine and dorzolamide–timolol eyedrops and was adequately controlled on medical therapy alone. Both haptics were in the bag, with the optic anterior to the capsulorhexis. Optical coherence tomography (OCT) and ultrasound biomicroscopy (UBM) showed iris–optic contact. Detry-Morel et al. speculate that secondary cataract displaced the poste- rior chamber IOL out of the capsular bag, causing iris chafing, and that the small Nd:YAG capsulotomy may have played a role in the accumulation of Elschnig pearls just behind the optic edge. I believe an inflammatory mechanism due to the re- lease of sequestered lens proteins into the vitreous by the laser capsulotomy is more likely than an IOL–iris chafing mechanism. Another possibility is recurrent idiopathic anterior uveitic glaucoma. My reasons are as follows: 1. The problem began late, 2 years after surgery, and was related to the laser capsulotomy. 2. It is difficult to understand how an in-the-bag IOL with angulated haptics, even with the optic anterior to the capsulorhexis, can exert enough pressure on the iris pigment epithelium to cause chafing and mechanical pigment dispersion. Upside down IOL implantation may make this possible, but the au- thors exclude this. Likewise, the possibility of pseu- dophacodonesis was excluded. 3. No hyperopic shift (expected if the IOL was pushed forward) was noted. 4. The glaucoma and anterior chamber cells were tran- sient. The problem resolved without any anatomical change. 5. There were no Krukenberg spindles, usually a sensi- tive sign of pigment dispersion. 6. The iris epithelial defects were noted within a month of symptoms; they usually require 6 to 12 months of iris chafing to develop. 2,3 7. Regarding the OCT and UBM findings: Demon- strating iris–optic contact is not good evidence of iris chafing; in normal eyes, the iris is often in contact with the IOL. More convincing evidence of IOL chafing, which UBM easily demonstrates, is IOL tilt 4,5 or haptic subluxation out of the bag and into the ciliary sulcus. 6 The authors speculate that Elschnig pearl prolifera- tion at the edge of the small posterior capsulotomy pushed the IOL anteriorly against the posterior iris surface. If so, why not attempt widening the capsulotomy to alleviate the forward pressure on the IOL optic? Understanding the mechanism of the glaucoma is important. If IOL chafing is the cause, surgery or im- mobilizing the iris with miotics would be the solution. If the mechanism is inflammatory, surgery may worsen the glaucoma; treatment would be antiinflam- matory medication. Russell Pokroy, MD Rehovot, Israel REFERENCES 1. Detry-Morel ML, Van Acker E, Pourjavan S, et al. Anterior seg- ment imaging using optical coherence tomography and ultra- sound biomicroscopy in secondary pigmentary glaucoma associated with in-the-bag intraocular lens. J Cataract Refract Surg 2006; 32:1866–1869 2. Mastropasqua L, Lobefalo L, Gallenga PE. Iris chafing in pseudo- phakia. Doc Ophthalmol 1994; 87:139–144 3. Mackool RJ. Pigmentary dispersion syndrome [letter]. J Cataract Refract Surg 2001; 27:1341; reply by R Wintle, M Austin, 1341– 1342 4. Loya N, Lichter H, Barash D, et al. Posterior chamber intraocular lens implantation after capsular tear: ultrasound biomicroscopy evaluation. J Cataract Refract Surg 2001; 27:1423–1427 5. Apple DJ, Reidy JJ, Googe JM, et al. A comparison of ciliary sul- cus and capsular bag fixation of posterior chamber intraocular lenses. Am Intra-Ocular Implant Soc J 1985; 11:44–63 6. LeBoyer RM, Werner L, Snyder ME, et al. Acute haptic-induced ciliary sulcus irritation associated with single-piece AcrySof intra- ocular lenses. J Cataract Refract Surg 2005; 31:1421–1427 REPLY: We appreciate Pokroy’s interest in our arti- cle and thank him for his pertinent comments and constructive suggestions. Pokroy has some doubt about the pathogenic mechanism we described based on the clinical examination and the anterior segment OCT (AS-OCT) and UBM images. He suggested that an inflammatory mechanism due to the release of sequestered lens proteins into the anterior chamber and the vitreous by the laser capsulotomy was more likely that an IOL–iris chafing mechanism. This hypothesis of hypertensive uveitis was quite plausible. We had considered it at the beginning of our management of the patient. However, the absence of cells in the vitreous and the chronic pigmented cells in the anterior chamber as well as the morphology of the iris atrophy and the trabecular hyperpigmentation are arguments against hypertensive uveitis. Moreover, 3 weeks of corticosteroid therapy was administered without a significant clinical effect and was therefore discontinued. The lack of a Krukenberg spindle, which has been less frequently described in secondary than in primary pigmentary dispersion syndrome (PDS), does not argue against our diagnosis. 1351 LETTERS J CATARACT REFRACT SURG - VOL 33, AUGUST 2007

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diopter AcrySofMA60 IOL (Alcon Laboratories) in thecapsular bag 2 years previously. The man complainedof intermittent, painless, blurred vision with intraocu-lar pressure reaching 40 mmHg and anterior chambercells, which began a few weeks after bilateral neody-mium:YAG (Nd:YAG) laser capsulotomies. He re-sponded well to atropine and dorzolamide–timololeyedrops and was adequately controlled on medicaltherapy alone. Both haptics were in the bag, with theoptic anterior to the capsulorhexis. Optical coherencetomography (OCT) and ultrasound biomicroscopy(UBM) showed iris–optic contact. Detry-Morel et al.speculate that secondary cataract displaced the poste-rior chamber IOL out of the capsular bag, causing irischafing, and that the small Nd:YAG capsulotomymayhave played a role in the accumulation of Elschnigpearls just behind the optic edge.

I believe an inflammatory mechanism due to the re-lease of sequestered lens proteins into the vitreous bythe laser capsulotomy is more likely than an IOL–irischafing mechanism. Another possibility is recurrentidiopathic anterior uveitic glaucoma. My reasons areas follows:

1. The problem began late, 2 years after surgery, andwas related to the laser capsulotomy.

2. It is difficult to understand how an in-the-bag IOLwith angulated haptics, even with the optic anteriorto the capsulorhexis, can exert enough pressure onthe iris pigment epithelium to cause chafing andmechanical pigment dispersion. Upside down IOLimplantation may make this possible, but the au-thors exclude this. Likewise, the possibility of pseu-dophacodonesis was excluded.

3. No hyperopic shift (expected if the IOL was pushedforward) was noted.

4. The glaucoma and anterior chamber cells were tran-sient. The problem resolvedwithout any anatomicalchange.

5. Therewere no Krukenberg spindles, usually a sensi-tive sign of pigment dispersion.

6. The iris epithelial defectswere notedwithin amonthof symptoms; they usually require 6 to 12 months ofiris chafing to develop.2,3

7. Regarding the OCT and UBM findings: Demon-strating iris–optic contact is not good evidence ofiris chafing; in normal eyes, the iris is often incontact with the IOL. More convincing evidence ofIOL chafing, which UBM easily demonstrates, isIOL tilt4,5 or haptic subluxation out of the bag andinto the ciliary sulcus.6

The authors speculate that Elschnig pearl prolifera-tion at the edge of the small posterior capsulotomypushed the IOL anteriorly against the posterior irissurface. If so, why not attempt widening the

capsulotomy to alleviate the forward pressure on theIOL optic?

Understanding the mechanism of the glaucoma isimportant. If IOL chafing is the cause, surgery or im-mobilizing the iris with miotics would be the solution.If the mechanism is inflammatory, surgery mayworsen the glaucoma; treatment would be antiinflam-matory medication.

Russell Pokroy, MDRehovot, Israel

REFERENCES1. Detry-Morel ML, Van Acker E, Pourjavan S, et al. Anterior seg-

ment imaging using optical coherence tomography and ultra-

sound biomicroscopy in secondary pigmentary glaucoma

associated with in-the-bag intraocular lens. J Cataract Refract

Surg 2006; 32:1866–1869

2. Mastropasqua L, Lobefalo L, Gallenga PE. Iris chafing in pseudo-

phakia. Doc Ophthalmol 1994; 87:139–144

3. Mackool RJ. Pigmentary dispersion syndrome [letter]. J Cataract

Refract Surg 2001; 27:1341; reply by R Wintle, M Austin, 1341–

1342

4. Loya N, Lichter H, Barash D, et al. Posterior chamber intraocular

lens implantation after capsular tear: ultrasound biomicroscopy

evaluation. J Cataract Refract Surg 2001; 27:1423–1427

5. Apple DJ, Reidy JJ, Googe JM, et al. A comparison of ciliary sul-

cus and capsular bag fixation of posterior chamber intraocular

lenses. Am Intra-Ocular Implant Soc J 1985; 11:44–63

6. LeBoyer RM, Werner L, Snyder ME, et al. Acute haptic-induced

ciliary sulcus irritation associated with single-piece AcrySof intra-

ocular lenses. J Cataract Refract Surg 2005; 31:1421–1427

1351LETTERS

J CATARACT REFRACT SURG

REPLY: We appreciate Pokroy’s interest in our arti-cle and thank him for his pertinent comments andconstructive suggestions. Pokroy has some doubtabout the pathogenic mechanism we described basedon the clinical examination and the anterior segmentOCT (AS-OCT) and UBM images. He suggested thatan inflammatory mechanism due to the release ofsequestered lens proteins into the anterior chamberand the vitreous by the laser capsulotomy was morelikely that an IOL–iris chafing mechanism.

This hypothesis of hypertensive uveitis was quiteplausible. We had considered it at the beginning ofour management of the patient. However, the absenceof cells in the vitreous and the chronic pigmented cellsin the anterior chamber as well as the morphology ofthe iris atrophy and the trabecular hyperpigmentationare arguments against hypertensive uveitis. Moreover,3 weeks of corticosteroid therapy was administeredwithout a significant clinical effect and was thereforediscontinued. The lack of a Krukenberg spindle, whichhas been less frequently described in secondary than inprimary pigmentary dispersion syndrome (PDS), doesnot argue against our diagnosis.

- VOL 33, AUGUST 2007

corneal power values above and below the 180-degreemeridian are used to calculate mean superior and infe-rior values, respectively. Sincemost keratoconus conesare inferotemporal and not purely inferior, some of thesteep values will be included in the calculation of thesuperior cornea.1 So, too, some of the flat values willfall inferior to the dividing line and be included in thecalculation of the inferior cornea. These stray valuesdilute the asymmetry of the I–S value, reducing its sen-sitivity to diagnose mild keratoconus, to compare theseverity of keratoconus, and to assess improvementafter treatment. This limitation of the I–S ratio is evengreater in corneas with temporal cones.

The L–U ratio uses the positive cylinder refractiveaxis obtained by refraction as the reference median, in-stead of the 180-degree meridian, to divide the corneainto halves.1 Five keratometric values are measured30 degrees apart at a 1.5 mm radius (3.0 mm zone)above and below this ‘‘tailored’’ reference median.The authors state that the L–U ratio was ‘‘significantlymore accurate than the I–S ratio after changes in kera-toconic eyes (unpublished data).‘‘ I would be inter-ested in seeing these data published.

Describing the severity of keratoconus numericallyhas proved difficult. Although we found the I–S ratioto be a useful index,3–5 the above-mentioned limita-tions are certainly significant. The newer L–U ratioappears to be a more effective index for assessing ker-atoconic corneas. To improve the reliability of and thecomparability between keratoconus studies, I stronglyrecommend the use of both L–U and I–S ratios in fu-ture keratoconus studies.

Russell Pokroy, MDRehovot, Israel

REFERENCES1. Chan CCK, Sharma M, Boxer Wachler BS. Effect of inferior-seg-

ment Intacs with and without C3-R on keratoconus. J Cataract

Refract Surg 2007; 33:75–80

2. Rabinowitz YS, Yang H, Brickman Y, et al. Videokeratography

database of normal human corneas. Br J Ophthalmol 1996;

80:610–616

3. Pokroy R, Levinger S, Hirsh A. Single Intacs segment for post-

laser in situ keratomileusis keratectasia. J Cataract Refract

Surg 2004; 30:1685–1695

4. Levinger S, Pokroy R. Keratoconus managed with Intacs; one-

1352 LETTERS

Because the patient consulted us after symptomaticepisodes of blurred vision, it was difficult to determinethe exact timing of the occurrence of the various events.We agree with Pokroy that the observed iris epithelialdefects generally require more than 2 months to de-velop, although this was quite impossible to confirm,especially if the iris–IOL contact and chafing weresevere. While as per Pokroy’s comments the presenceof chronic anterior chamber cells may be the sign ofuveitis of self-limited evolution, it may also be relatedto the mechanical effects of the IOL.

The postoperative evolution of the patient’s refrac-tion was unknown. The forward displacement of theIOL, which was probably too mild to induce signifi-cant shallowing of the anterior chamber, should haveinduced a myopic shift.

Regarding the AS-OCT and UBM findings, the ana-tomical conditions were similar in both eyes, whereasAS-OCT and UBM did not show any iris–optic IOLcontact in the fellow eye. Unfortunately, photographsshowing the circular peripupillary iris atrophy opti-mally, which was quite different than those observedin PDS in phakic eyes, exactly faced the IOL andclearly reflected contact and iris–IOL chafing, werenot taken for technical reasons.

As Pokroy outlined, the treatment of this casereport was very challenging. We excluded mioticmedications because of the high myopia and a historyof retinal detachment in the fellow eye. With thisconcern in mind and the relatively self-limited courseof the disease, we did not consider a potentially riskyIOL surgery. Because the optic of the IOL was fixatedin front of the capsulorhexis and unable to movebackward again, it would also have probably beentoo late to consider enlargement of the posteriorcapsulorhexis. Careful laser iridotomy might havebeen considered to alleviate the IOL–iris chafingmechanism.

We acknowledge Pokroy’s comment about theimportance of understanding the mechanism of oc-ular hypertension and/or glaucoma before consider-ing any treatment.dMichele L. Detry-Morel, MD,Emmanuel Van Acker, MD, Sayeh Pourjavan,Natacha Levi, MD, Patrick De Potter, MD, PhD

Lower–upper corneal power asymmetry ratiofor keratoconus

I commend Chan et al.1 on their description and useof a new corneal topographic index for the quantifica-tion of keratoconus severity; that is, the lower–upper(L–U) ratio. This is a modification of the well-acceptedRabinowitz inferior–superior (I–S) ratio,which dividesthe cornea into inferior and superior halves using the180-degree meridian.2 Thereafter, 15 paracentral

year results. Arch Ophthalmol 2005; 123:1308–1314

5. Pokroy R, Levinger S. Intacs adjustment surgery for keratoconus.

J Cataract Refract Surg 2006; 32:986–992

REPLY: We thank Pokroy for his positive commentsabout the L–U ratio, which came from our observationthat cones are more often placed obliquely than di-rectly inferiorly. Hence, the I–S ratio may not ade-quately quantify the degree of keratoconus in many

J CATARACT REFRACT SURG - VOL 33, AUGUST 2007