Dear Editor,
We read with great interest the study conducted by Yu X et al.1 comparing the efficacy of augmented surgical doses of surgery and Botulinum Toxin A injection for Acute acquired concomitant esotropia (AACE).
AACE has been on the rise with the advent of digital education for children, smartphones and change in lifestyles for both adults and children and hence this work is of particular interest to us.
We wish to report outcomes from our unpublished series of acquired esotropia. We retrospectively analyzed 29 patients of AACE, over a 17 month period between April 2022 and September 2023. As per protocol, we used surgical doses suggested by standard tables and did not use augmentation. The mean angle of deviation was 43.09 9.32 PD at 6m and 46.31 9.8 PD at 33cm preoperatively. The mean dose response without augmentation we achieved was 3.12 0.62 PD/mm and we achieved surgical success in 28 patients. The post operative final angles of deviation were 3.33 5.81 PD at 6m and 4.05-6.64 PD at 33cm at the last follow up. We used similar criteria of surgical success as Yu X et al.
Kim et al also report successful surgical outcomes in their subset of AACE patients using standard doses from Park’s tables.3
Augmented surgery has also been done by either increasing the amount of recession or resection and has resulted in good motor and sensory outcomes4,5
Yu et al recommend augmenting their surgical dose by...
Dear Editor,
We read with great interest the study conducted by Yu X et al.1 comparing the efficacy of augmented surgical doses of surgery and Botulinum Toxin A injection for Acute acquired concomitant esotropia (AACE).
AACE has been on the rise with the advent of digital education for children, smartphones and change in lifestyles for both adults and children and hence this work is of particular interest to us.
We wish to report outcomes from our unpublished series of acquired esotropia. We retrospectively analyzed 29 patients of AACE, over a 17 month period between April 2022 and September 2023. As per protocol, we used surgical doses suggested by standard tables and did not use augmentation. The mean angle of deviation was 43.09 9.32 PD at 6m and 46.31 9.8 PD at 33cm preoperatively. The mean dose response without augmentation we achieved was 3.12 0.62 PD/mm and we achieved surgical success in 28 patients. The post operative final angles of deviation were 3.33 5.81 PD at 6m and 4.05-6.64 PD at 33cm at the last follow up. We used similar criteria of surgical success as Yu X et al.
Kim et al also report successful surgical outcomes in their subset of AACE patients using standard doses from Park’s tables.3
Augmented surgery has also been done by either increasing the amount of recession or resection and has resulted in good motor and sensory outcomes4,5
Yu et al recommend augmenting their surgical dose by 15 PD for AACE. It is interesting to note similar outcomes in two different population groups and with two different approaches and we wonder if this could be attributed to dose response affect in different racial backgrounds.
.
References
1. Yu X, Pan W, Tang X, et al. Br J Ophthalmol. 2023. 0:1–5. doi:10.1136/bjo-2023-323646
2. Rosenbaum AL, Santiago AP. Clinical Strabismus Management: Principles and Surgical techniques. 1st Edition. Philadelphia, Pennsylvania. W.B. Saunders Company. 1999. Appendix: Surgical Tables 552-554. ISBN 0-7216-7673-1.
3. Kim, D.H., Noh, H.J. Surgical outcomes of acute acquired comitant esotropia of adulthood. BMC Ophthalmol 21, 45 (2021).
4. Lekskul A, Chotkajornkiat N, Wuthisiri W, Tangtammaruk P. Acute Acquired Comitant Esotropia: Etiology, Clinical Course, and Management. Clin Ophthalmol. 2021 Apr 15;15:1567-1572
5. Shi M, Zhou Y, Qin A, Cheng J, Ren H. Treatment of acute acquired concomitant esotropia. BMC Ophthalmol. 2021 Jan 6;21(1):9.
Dear Editor, we read with interest the study of Hilely and coworkers, describing a new condition which they referred to as pachyvitelliform maculopathy. Their study clearly demonstrates the association between pachychoroid features and adult vitelliform lesions (AVLs).1 Two previous reports by our teams may stregthen their hypothesis of a relationship between the two conditions. In cuticular drusen, we have shown that vitelliform detachments occur significantly more often in eyes with a thick choroid, and we suggested that the choroidal vasculature could play a role in the occurrence of macular detachments in patients with cuticular drusen, leading to accumulation of photreceptors debris and deposits.2 More recently, we report a series of 49 eyes with hyperreflective vertical lines diagnosed on B-scans of spectral-domain optical coherence tomography. Twenty-four eyes presented with AVLs related to adult vitelliform dystrophy or pattern dystrophy. We were surprised that, in 14 cases out of 24, signs of pachychoroid were present. We suggested that further studies were needed to better understand this relationship.3 So we fully agree in that the pachychoroid syndrome may interfere with the metabolism of the retinal pigment epithelium and the phagocytosis process, leading to accumulation of photoreceptors debris. We really thank Hilely and coworkers for their convincing step towards a better recognition of this curious association.
Dear Editor, we read with interest the study of Hilely and coworkers, describing a new condition which they referred to as pachyvitelliform maculopathy. Their study clearly demonstrates the association between pachychoroid features and adult vitelliform lesions (AVLs).1 Two previous reports by our teams may stregthen their hypothesis of a relationship between the two conditions. In cuticular drusen, we have shown that vitelliform detachments occur significantly more often in eyes with a thick choroid, and we suggested that the choroidal vasculature could play a role in the occurrence of macular detachments in patients with cuticular drusen, leading to accumulation of photreceptors debris and deposits.2 More recently, we report a series of 49 eyes with hyperreflective vertical lines diagnosed on B-scans of spectral-domain optical coherence tomography. Twenty-four eyes presented with AVLs related to adult vitelliform dystrophy or pattern dystrophy. We were surprised that, in 14 cases out of 24, signs of pachychoroid were present. We suggested that further studies were needed to better understand this relationship.3 So we fully agree in that the pachychoroid syndrome may interfere with the metabolism of the retinal pigment epithelium and the phagocytosis process, leading to accumulation of photoreceptors debris. We really thank Hilely and coworkers for their convincing step towards a better recognition of this curious association.
Salomon Y Cohen, A Gaudric, Sarah Mrejen
Centre Ophtalmologique d’Imagerie et de Laser, Paris, France
References
1. Hilely A, Au A, Lee WK, Fogel Levin M, et al. Pachyvitelliform maculopathy: an optical coherence tomography analysis of a novel entity. Br J Ophthalmol. 2023 Jul 14:bjo-2022-322553.
2. Mrejen-Uretsky S, Ayrault S, Nghiem-Buffet S, et al. Choroidal thickening in patients with cuticular drusen combined with vitelliform macular detachment. Retina. 2016;36(6):1111-8.
3. Amoroso F, Mrejen S, Pedinielli A, et al. Intraretinal hyperreflective lines. Retina. 2021;41(1):82-92.
We read with considerable attention the manuscript by Hilely et al. entitled “Pachyvitelliform maculopathy: an optical coherence tomography analysis of a novel entity.”1 We would like to compliment the Authors on their great effort and excellent figures.
Hilely and associated introduced a novel clinical entity named pachyvitelliform maculopathy (PVM). It consisted of the association between acquired vitelliform lesion (AVL) and pachychoroid disease spectrum (PDS) features, including pachychoroid (choroidal thickness > 250 μm), pachyvessels (dilated Haller vessels), and inner choroid thinning. In detail, a yellowish hyperreflective lesion overlayed a thick choroid and pachyvessels. In contrast to other forms PDS,2 PVM displayed no subretinal (SRF) or intraretinal fluid (IRF) and neovascularization. Furthermore, cases of pachychoroid and drusen (medium, large, cuticular, pseudo reticular, and subretinal drusenoid deposits) were excluded. This condition was described in 60 years older subjects with electro-oculogram within normal range and with a negative genetic test, although performed in a minority of the cohort.
We would like to have the thoughts about the following issue that Hilely and colleagues ought to address. Although the Authors stated that this was the first description of PVM, previous papers discussed the aforementioned association between PDS and vitelliform lesions. In detail, Spaide described three cases (two monoliteral, and one bilateral) o...
We read with considerable attention the manuscript by Hilely et al. entitled “Pachyvitelliform maculopathy: an optical coherence tomography analysis of a novel entity.”1 We would like to compliment the Authors on their great effort and excellent figures.
Hilely and associated introduced a novel clinical entity named pachyvitelliform maculopathy (PVM). It consisted of the association between acquired vitelliform lesion (AVL) and pachychoroid disease spectrum (PDS) features, including pachychoroid (choroidal thickness > 250 μm), pachyvessels (dilated Haller vessels), and inner choroid thinning. In detail, a yellowish hyperreflective lesion overlayed a thick choroid and pachyvessels. In contrast to other forms PDS,2 PVM displayed no subretinal (SRF) or intraretinal fluid (IRF) and neovascularization. Furthermore, cases of pachychoroid and drusen (medium, large, cuticular, pseudo reticular, and subretinal drusenoid deposits) were excluded. This condition was described in 60 years older subjects with electro-oculogram within normal range and with a negative genetic test, although performed in a minority of the cohort.
We would like to have the thoughts about the following issue that Hilely and colleagues ought to address. Although the Authors stated that this was the first description of PVM, previous papers discussed the aforementioned association between PDS and vitelliform lesions. In detail, Spaide described three cases (two monoliteral, and one bilateral) of central serous chorioretinopathy (before the introduction of PDS definition) that slowly (range: 6 months - 5.5 years) developed sub-retinal yellowish material similar to that seen in adult-onset foveal vitelliform dystrophy (AOFVD) in absence of exudation.3 Furthermore, also Hilely et al. described this lesion appeared hyperfluorescent on fundus autofluorescence, suggesting that its content was made of lipofuscin-like AOFVD.4 Spaide hypothesized that the development of the yellowish deposit in CSC eyes and AOFVD occurred after resorption of the subretinal fluid as a late step of a process not completely understood. However, this study lacked optical coherence tomography (OCT) analysis, so it’s not possible to exclude with certainty that these cases did not present any signs of SRF, as declared by Spaide et al.3 Freund and colleagues then examined the multimodal imaging appearance of AVL, including structural OCT. The group reported two cases of CSC (again before the introduction of the PDS definition) and AVL, with one of them showing no SRF. Interestingly, no early or unilateral AVL showed SRF also in the fellow eye, indicating that the formation of the vitelliform lesion comes first before the occurrence of SRF.5 Subsequently, Soman et al.6 described as first a case of bilateral AVL and pachychoroid, that in one eye was complicated by macular neovascularization (MNV). A noteworthy aspect of this case of pachychoroid neovasculopathy was the initial description of bilateral vitelliform lesions without concomitant retinal fluid, followed in the left eye by the progression from a nonexudative to an exudative MNV combined with reabsorption, and subsequent deposition of AVL in a different location.6 Recently, the association between AVL and a form of PDS (i.e. peripapillary pachychoroid syndrome) was reported. However, all these cases showed IRF, and in a minority of cases also SRF, as these are typical features of this condition. 7
Given all this evidence, it would be difficult to conclude that the Authors reported a new clinical entity. The association between different forms of PDS and AVL was yet reported, even if in sporadic series. The Authors had the merit of having better characterized this peculiar form of PDS associated with AVL in the new classifications of PDS subtypes. However, it cannot be excluded with certainty that the Authors reported cases of CSC after the reabsorption of leakage fluid, similar to the aforementioned previous evidence. We are interested in the Authors' thoughts on the matter.
References
1. Hilely A, Au A, Lee WK, et al. Pachyvitelliform maculopathy : an optical coherence tomography analysis of a novel entity. Br J Ophthalmol. 2023;0:1-7. doi:10.1136/bjo-2022-322553
2. Van Dijk EHC, Boon CJF. Serous business: Delineating the broad spectrum of diseases with subretinal fluid in the macula. Prog Retin Eye Res. 2021;84:100955. doi:10.1016/j.preteyeres.2021.100955
3. Spaide RF. Deposition of yellow submacular material in central serous chorioretinopathy resembling adult-onset foveomacular vitelliform dystrophy. Retina. 2004;24(2):301-304. doi:10.1097/00006982-200404000-00019
4. Spaide RF, Noble K, Morgan A, Freund KB. Vitelliform Macular Dystrophy. 2006;2. doi:10.1016/j.ophtha.2006.03.023
5. Freund KB, Laud K, Lima LH, Spaide RF, Zweifel S, Yannuzzi LA. Acquired Vitelliform Lesions. Retina. 2011;31(1):13-25. doi:10.1097/iae.0b013e3181ea48ba
6. Soman M, Iqbal S, Sheth JU, Meleth P, Nair U. Progression of Subclinical Pachychoroid Neovasculopathy to an Active Neovascularization in the Presence of Acquired Vitelliform Lesions. Case Rep Ophthalmol Med. 2021;2021(c):1-8. doi:10.1155/2021/3098420
7. Barequet D, Iglicki M, Meshi A, Loewenstein A, Goldstein M, Zur D. ACQUIRED VITELLIFORM LESIONS: A Novel Finding in Eyes with Peripapillary Pachychoroid Syndrome. Retina. 2022;42(5):949-956. doi:10.1097/IAE.0000000000003403
We thank Dr. Carkeet for his comments on our paper,1 which is now over 15 years old.
As discussed with Dr. Carkeet in personal correspondence recently, the discrepancy between his results and ours occurred because we simplified the 1 exam/year and 3 exam/years conditions by linearly scaling the outputs from the 2 exam/year condition. We repeated the simulations under the conditions Dr. Carkeet has outlined, and we agree with the result. The simulations yield approximately the same time required to detect the various rates of change for 2 exams per year, and slightly different values for 1 and 3 exams per year. He has pointed out discrepancies in the 1 and 3 exam per year conditions which appear large only in extreme conditions and are not realistic in clinical practice, for example, detecting a -0.25 dB/y change with high variability, where we estimated 30 years and Dr. Carkeet estimated 18 years.
In the final analysis simulations are only simulations that can be made with conditions assumed to reflect reality. The precision with which these estimates is made can be low. Ultimately, the message in our paper was that it takes a long time to detect a small amount of change if visual field results are variable and the testing frequency is low.
Our paper has been used to inform guidelines from various organizations and is based on one of the key messages of the paper, i.e., that ruling out fast progression (worse -2 dB/y or worse) requires 6 visual...
We thank Dr. Carkeet for his comments on our paper,1 which is now over 15 years old.
As discussed with Dr. Carkeet in personal correspondence recently, the discrepancy between his results and ours occurred because we simplified the 1 exam/year and 3 exam/years conditions by linearly scaling the outputs from the 2 exam/year condition. We repeated the simulations under the conditions Dr. Carkeet has outlined, and we agree with the result. The simulations yield approximately the same time required to detect the various rates of change for 2 exams per year, and slightly different values for 1 and 3 exams per year. He has pointed out discrepancies in the 1 and 3 exam per year conditions which appear large only in extreme conditions and are not realistic in clinical practice, for example, detecting a -0.25 dB/y change with high variability, where we estimated 30 years and Dr. Carkeet estimated 18 years.
In the final analysis simulations are only simulations that can be made with conditions assumed to reflect reality. The precision with which these estimates is made can be low. Ultimately, the message in our paper was that it takes a long time to detect a small amount of change if visual field results are variable and the testing frequency is low.
Our paper has been used to inform guidelines from various organizations and is based on one of the key messages of the paper, i.e., that ruling out fast progression (worse -2 dB/y or worse) requires 6 visual fields in the first 2 years if the exams are equally spaced. None of the other testing frequencies/amounts of change in our paper have been incorporated into the guidelines. Since our paper was published, others have built upon our work and performed simulations with more nuanced assumptions,2 3 such as clustering exam frequency and spacing. Nonetheless, this key guideline, that is requires 6 examinations in the first 2 years to rule out fast progression remains true. Whether the real number is 5 or 6 or 7 is immaterial. Given that in many jurisdictions, patients diagnosed with glaucoma receive less than 1 exam per year,4 5 arguing about subtleties in simulation conditions that impact marginal conditions seems trivial.
References
1. Chauhan BC, Garway-Heath DF, Goni FJ, et al. Practical recommendations for measuring rates of visual field change in glaucoma. Br J Ophthalmol 2008;92(4):569-73. doi: 10.1136/bjo.2007.135012 [published Online First: 20080122]
2. Crabb DP, Garway-Heath DF. Intervals between visual field tests when monitoring the glaucomatous patient: wait-and-see approach. Invest Ophthalmol Vis Sci 2012;53(6):2770-6. doi: 10.1167/iovs.12-9476 [published Online First: 20120517]
3. Wu Z, Saunders LJ, Daga FB, et al. Frequency of Testing to Detect Visual Field Progression Derived Using a Longitudinal Cohort of Glaucoma Patients. Ophthalmology 2017;124(6):786-92. doi: 10.1016/j.ophtha.2017.01.027 [published Online First: 20170306]
4. Fung SS, Lemer C, Russell RA, et al. Are practical recommendations practiced? A national multi-centre cross-sectional study on frequency of visual field testing in glaucoma. Br J Ophthalmol 2013;97(7):843-7. doi: 10.1136/bjophthalmol-2012-302903 [published Online First: 20130423]
5. Stagg BC, Stein JD, Medeiros FA, et al. The Frequency of Visual Field Testing in a US Nationwide Cohort of Individuals with Open-Angle Glaucoma. Ophthalmol Glaucoma 2022;5(6):587-93. doi: 10.1016/j.ogla.2022.05.002 [published Online First: 20220520]
We thank Dr Velez-Montoya and colleagues for their interest in our study.1 We reported that there was an increase in the prevalence of endophthalmitis after vitrectomy in Japan and found that it was probably related to the face masks during the COVID period.2 Although the cause for the increase definitively determined, we need to report these findings to the ophthalmologic community to alert them of this possibility.
First, we address the indicated point, “the definition of postoperative endophthalmitis was not rigorous”. We used the definition of the Endophthalmitis Vitrectomy Study group.3 Although this definition is relatively old, many subsequent studies have used it, and it has the advantage that our findings could be compared to these other studies with the same definition.
They also stated that the latest studies have shown that the sclerotomies after a pars plana vitrectomy seal within 15 days after the surgery even after a suture-less closure. Thus, the site of the incision was unlikely the entry port for the infectious micro-organisms after that time. This is generally true but the cause of infectious endophthalmitis after vitrectomy is complex. Because the cause of infectious endophthalmitis is varied, it is not surprising that anything can happen with postoperative endophthalmitis. For example, it is possible for a patient to inadvertently touch the eye in the early postoperative period and cause the incision to open. Once...
We thank Dr Velez-Montoya and colleagues for their interest in our study.1 We reported that there was an increase in the prevalence of endophthalmitis after vitrectomy in Japan and found that it was probably related to the face masks during the COVID period.2 Although the cause for the increase definitively determined, we need to report these findings to the ophthalmologic community to alert them of this possibility.
First, we address the indicated point, “the definition of postoperative endophthalmitis was not rigorous”. We used the definition of the Endophthalmitis Vitrectomy Study group.3 Although this definition is relatively old, many subsequent studies have used it, and it has the advantage that our findings could be compared to these other studies with the same definition.
They also stated that the latest studies have shown that the sclerotomies after a pars plana vitrectomy seal within 15 days after the surgery even after a suture-less closure. Thus, the site of the incision was unlikely the entry port for the infectious micro-organisms after that time. This is generally true but the cause of infectious endophthalmitis after vitrectomy is complex. Because the cause of infectious endophthalmitis is varied, it is not surprising that anything can happen with postoperative endophthalmitis. For example, it is possible for a patient to inadvertently touch the eye in the early postoperative period and cause the incision to open. Once opened, the scleral wound becomes a point of entry for infectious organisms. Additionally, the vitreous wick syndrome has been reported to occur especially after sutureless vitrectomy.4 Exposure to oral bacteria through masks can also result in infections. Considering the fatigue of the surgical team (human error) at the peak of the COVID epidemic, it is understandable that the source of infection most likely was during the vitrectomy. Nevertheless, other possibilities must be considered. Thus, the present definition of endophthalmitis, even in cases of infection after 42 days, is meaningful
Second, it is fair to point out that bacteria such as Streptococcus mitis are usually low pathogenic or opportunistic pathogens. However, S. mitis was the second most common organism found in cultures in post vitrectomy endophthalmitis.5 Exposure to exhaled air containing endemic oral bacteria for more than a certain amount of time can cause this.
Third, regarding Velez-Montoya and colleagues’ statement, “the results observed for the prevalence of postoperative endophthalmitis in the phacoemulsification-only group is not consistent with the main hypothesis”. We explained these findings as follows in the original paper. There was no difference in the frequency of endophthalmitis after cataract surgery before and after the masking period. Cataract surgery and vitreous surgery are different procedures. The incidence of endophthalmitis was significantly higher after vitrectomy, even when exposed to the same species and dosages.2 It is because the defense system against pathogenic microorganisms is weaker in the vitreous than in the anterior chamber.6 This is possibly the reason why an increase was detected only in the post-vitrectomy cases. This may also be related to the fact that the concentration of bacteria around the eye was somewhat increased by the strict mask wearing. This explains our finding that the incidence of endophthalmitis is the same in cataract surgery before and during COVID19-mask period, but is higher in vitrectomy during the COVID19-mask period. This is consistent with our assumption that the masked period is associated with a higher incidence of infective endophthalmitis after vitrectomy.
We again thank Dr Velez-Montoya and colleagues for their advice and the British Journal of Ophthalmology for providing us with a space to share our comments with the medical community.
References
1. Velez-Montoya, Raul, et al. Letter to the editor on "Increased incidence of endophthalmitis after vitrectomy relative to face mask wearing during COVID-19 pandemic.". Brit J Ophthalmol 2023
2. Sakamoto T, Terasaki H, Yamashita T, Shiihara H, Funatsu R, Uemura A; Japanese Retina and Vitreous Society. Increased incidence of endophthalmitis after vitrectomy relative to face mask wearing during COVID-19 pandemic. Br J Ophthalmol. 2022 Jun 21:bjophthalmol-2022-321357. doi: 10.1136/bjophthalmol-2022-321357. Epub ahead of print. PMID: 35728937.
3. Results of the Endophthalmitis Vitrectomy Study. A randomized trial of immediate vitrectomy and of intravenous antibiotics for the treatment of postoperative bacterial endophthalmitis. Endophthalmitis Vitrectomy Study Group. Arch Ophthalmol. 1995;113:1479-1496.
4. Venkatesh P, Verma L, Tewari H. Posterior vitreous wick syndrome: a potential cause of endophthalmitis following vitreo-retinal surgery. Med Hypotheses. 2002 Jun;58(6):513-5. doi: 10.1054/mehy.2001.1490. PMID: 12323120.
5. Li AL, Wykoff CC, Wang R, Chen E, Benz MS, Fish RH, Wong TP, Major JC Jr, Brown DM, Schefler AC, Kim RY, OʼMalley RE. Endophthalmitis after intravitreal injection: Role of Prophylactic Topical Ophthalmic Antibiotics. Retina. 2016 Jul;36(7):1349-56. doi: 10.1097/IAE.0000000000000901. PMID: 26655622.
6. Shockley RK, Jay WM, Fishman PH, Aziz MZ, Rissing JP. Effect of inoculum size on the induction of endophthalmitis in aphakic rabbit eyes. Acta Ophthalmol (Copenh). 1985;63:35-38.
Chauhan and co-workers [1] have provided Table 1, showing times taken to detect significant field progression with 80% power, based on a number of modelling parameters: frequency of examinations, rate of field progression, intrasession variability of field assessment. They have also provided Table 2 showing the number of annual eye examinations required to detect different total visual field changes, for different time periods, and for moderate variability. I have checked the calculations of Chauhan and co-workers, using Monte Carlo modelling, assuming a one-tailed significance value of 0.025. Of the 36 outcome values in Table 1, 33 are incorrect. Of the 12 outcome values in Table 2, 11 are incorrect.
Chauhan and co-workers have made 2 main errors in their calculations for Table 1. The first is in applying their estimates of power. The curves shown in Figure 2 (statistical power plotted against number of field examinations) are appropriate for the case of 2 field examinations per year, but Chauhan and co-workers appear to have incorrectly also used them for the cases of 1 examination per year and 3 examinations per year. Separate sets of curves should have been calculated for those conditions. The effect on Table 1 is that the time taken to detect a field change is incorrectly reported as being inversely proportional to the number of examinations per year. This anomalous relationship was commented on by Albert Alm in his 2008 Rapid Response, “Is a field every 4...
Chauhan and co-workers [1] have provided Table 1, showing times taken to detect significant field progression with 80% power, based on a number of modelling parameters: frequency of examinations, rate of field progression, intrasession variability of field assessment. They have also provided Table 2 showing the number of annual eye examinations required to detect different total visual field changes, for different time periods, and for moderate variability. I have checked the calculations of Chauhan and co-workers, using Monte Carlo modelling, assuming a one-tailed significance value of 0.025. Of the 36 outcome values in Table 1, 33 are incorrect. Of the 12 outcome values in Table 2, 11 are incorrect.
Chauhan and co-workers have made 2 main errors in their calculations for Table 1. The first is in applying their estimates of power. The curves shown in Figure 2 (statistical power plotted against number of field examinations) are appropriate for the case of 2 field examinations per year, but Chauhan and co-workers appear to have incorrectly also used them for the cases of 1 examination per year and 3 examinations per year. Separate sets of curves should have been calculated for those conditions. The effect on Table 1 is that the time taken to detect a field change is incorrectly reported as being inversely proportional to the number of examinations per year. This anomalous relationship was commented on by Albert Alm in his 2008 Rapid Response, “Is a field every 4 month a significant improvement over a field every 6 months?”. He wrote, “… increasing the duration is much more efficient than increasing the frequency of examinations. Thus, 5 examinations in 1.7 years will not be able to detect the same slope as 5 examinations in 5 years!” My calculations for the values in Table 1 show that increasing examination frequency, from once per year to 3 times per year, reduces time to detect a field change to between 71% and 50%, not 33% as implied by the original paper.
The second error made by Chauhan and co-workers is in converting from the number of fields (S) required to the duration required (D) for a given annual frequency of testing (f). From equation 5 in another paper,[2] this relationship is: D=(S-1)/f. Chauhan and co-workers appear to have used D=S/f.
In Table 1, three values are correct. One of those correct values, that it takes 2 years to detect fast progression (MD rate =-2dB/Year) with moderate field variability (SD=1dB) with 3 examinations/year, seems to be the basis for the paper’s recommendation that “six visual field examinations should be performed in the first 2 years.” This is slightly incorrect. A testing frequency of 3 examinations per year over 2 years will yield 7 examinations.
Table 2 contains significant errors. For example, its results imply that detecting a total field change of 1 dB will require between 15 and 21 measurements with SD= 1dB, depending on the number of years measurements are spread over. My calculations give an estimate of 95 total measurements required (irrespective of the time span).
This paper has been, and continues to be, influential. For example, Table 1 has been included in clinical glaucoma management guidelines.[3] The journal’s article metrics show 371 citations for the paper at the time of writing. Yet, the paper incorrectly overemphasises the value of increasing visual field test frequency. That is a core message for the paper. Given the paper’s influence those errors should be corrected.
References
1. Chauhan BC, Garway-Heath DF, Goñi FJ, et al. Practical recommendations for measuring rates of visual field change in glaucoma. Br J Ophthalmol 2008;92(4):569-73. doi: 10.1136/bjo.2007.135012 [published Online First: 2008/01/24]
2. Schlesselman JJ. Planning a longitudinal study. II. Frequency of measurement and study duration. J Chronic Dis 1973;26(9):561-70. doi: 10.1016/0021-9681(73)90061-1
3. NHMRC. NHMRC Guidelines for the screening, prognosis, diagnosis, management and prevention of glaucoma 2010: National Health and Medical Research Council, Canberra., 2010.
We read the paper on non-invasive intracranial pressure determination by Zhang et al(1) with great interest and hope. We fully agree that the search for non-invasive intracranial pressure (ICP) evaluations is of high importance and should be continued. The Bland-Altman plot showing the difference between predicted and intracranially measured pressure looks very impressive. There are, however, still a few points and limits we would like to address concerning the anatomy of the optic nerve, the optic canal, and the basic concept the authors used.
Cerebrospinal fluid (CSF) from the intracranial subarachnoid spaces and the subarachnoid space of the optic nerve (SAS -ON) communicate via the optic canal. Using three-dimensional reconstruction of the optic canal in normal tension glaucoma (NTG) patients, this was found to be narrower than in an age-related cohort of normals,(2) thus questioning the patency of the CSF pathway between the pituitary cistern and the SAS-ON. Further, optic canal dimensions in a normal population are quite variable amongst individuals, and even between orbits within the same individual.(3) These facts largely influence the results the authors present. Further, studies in patients with NTG and patients with elevated ICP (such as patients with idiopathic intracranial hypertension) were shown to have developed an optic nerve sheath compartment syndrome. In such cases, the CSF dynamics between the intracranial CSF and the CSF in...
We read the paper on non-invasive intracranial pressure determination by Zhang et al(1) with great interest and hope. We fully agree that the search for non-invasive intracranial pressure (ICP) evaluations is of high importance and should be continued. The Bland-Altman plot showing the difference between predicted and intracranially measured pressure looks very impressive. There are, however, still a few points and limits we would like to address concerning the anatomy of the optic nerve, the optic canal, and the basic concept the authors used.
Cerebrospinal fluid (CSF) from the intracranial subarachnoid spaces and the subarachnoid space of the optic nerve (SAS -ON) communicate via the optic canal. Using three-dimensional reconstruction of the optic canal in normal tension glaucoma (NTG) patients, this was found to be narrower than in an age-related cohort of normals,(2) thus questioning the patency of the CSF pathway between the pituitary cistern and the SAS-ON. Further, optic canal dimensions in a normal population are quite variable amongst individuals, and even between orbits within the same individual.(3) These facts largely influence the results the authors present. Further, studies in patients with NTG and patients with elevated ICP (such as patients with idiopathic intracranial hypertension) were shown to have developed an optic nerve sheath compartment syndrome. In such cases, the CSF dynamics between the intracranial CSF and the CSF in the SAS-ON differ significantly. This was proven by applying computer-assisted cisternography, diffusion-weighted MRI sequences and gradients of biochemical CSF proteins.(4-6)
In Zhang’s study, CSF pressures (CSFP) larger than 30 mm Hg were excluded. The majority of the patients in whom CSFP needs to be known are those with markedly elevated ICP. Therefore, this study should have been expanded to this group. As the compliance to pressure in the optic nerve sheath is most likely notlinear, this adds a further difficulty to measuring methods.
The authors found that CSF pressure was more significantly correlated with the area of the optic nerve sheath subarachnoid space than with the optic nerve sheath diameter. In an idealized fashion the optic nerve subarachnoid space resembles an annulus with a fractal circumference. The area A itself is not homogeneously filled with CSF but is interspersed with an interindividually variable amount of space-occupying trabeculae. The diameter in an annulus – compared to a circle - is represented twice in the formula for the area. Therefore, the diameter is involved in the SAS area as well. Its therefore difficult to understand why using the area instead of the diameter should render more accurate calculations, especially when the diameter is represented twice in the formula:
A total = π/4 (D2 -d2 ) - A trabecula = π (R2 - r2) - A trabecula
Our prior experience with formulae utilizing biophysical data such as body mass index (BMI), diastolic blood pressure (DBP), and age – all factors known to correlate to CSF pressure to variable degrees – were that they are quite poor at predicting actual CSF pressure.(7) The study excluded the analysis of formulae that utilized anatomic measures of MRI-determined optic nerve sheath width. However, as Zhang’s study is utilizing a similar method except with ultrasonographic determination of nerve sheath width, it would be assumed that the strongest predictor of CSF pressure would be the optic nerve sheath width. This subject has been repeatedly studied, and it does not seem that ultrasonographic evaluation of the optic nerve sheath diameter has ever been able to determine accurate estimates of true CSF pressures, but mostly the determination of normal versus elevated.(8-10)
Lastly, ultrasonography is a subjective method that depends on the user’s ability and reliability. In a study comparing optic nerve sheath diameter measurement between computed tomography, magnetic resonance imaging and ultrasound there was a good comparability between computed tomography and magnetic resonance imaging while the comparability between ultrasound and computed tomography or magnetic resonance tomography seems to be less reliable.(11)
We highly encourage efforts to expand our knowledge of the interrelation of cerebrospinal fluid and ophthalmic disease. But our desire to increase accessibility to study this by using formulae (in which the relationship between the variables is not understood) as opposed to current gold standard measurements of CSF pressure determination should not lead us to the path of using doubtful formulae that will confuse our body of literature.
References:
1) Non-invasive intracranial pressure estimation using ultrasonographic measurement of area of optic nerve subarachnoid space.Zhang Y, Cao K, Pang R, Wang N, Qu X, Kang J, Wang N, Liu H. Br J Ophthalmol. 2022 Aug 24:bjophthalmol-2022-321065.
2) The Optic Canal: A Bottleneck for Cerebrospinal Fluid Dynamics in Normal-Tension Glaucoma?Pircher A, Montali M, Berberat J, Remonda L, Killer HE. Front Neurol. 2017 Feb 23;8:47
3) Evaluation of optic canal anatomy and symmetry. Zhang X, Lee Y, Olson D, Fleischman D. BMJ Open Ophthalmology 2019;4:e000302
4) Cerebrospinal fluid dynamics between the intracranial and the subarachnoid space of the optic nerve. Is it always bidirectional? Killer HE, Jaggi GP, Flammer J, Miller NR, Huber AR, Mironov A. Brain. 2007 Feb;130(Pt 2):514-20
5) Case Report: Cerebrospinal Fluid Dynamics in the Optic Nerve Subarachnoid Space and the Brain Applying Diffusion Weighted MRI in Patients With Idiopathic Intracranial Hypertension-A Pilot Study. Berberat J, Pircher A, Gruber P, Lovblad KO, Remonda L, Killer HE. Front Neurol. 2022 Apr 15;13:862808
6) The optic nerve: a new window into cerebrospinal fluid composition? Killer HE, Jaggi GP, Flammer J, Miller NR, Huber AR. Brain. 2006 Apr;129(Pt 4):1027-30
7) Analysis of cerebrospinal fluid pressure estimation using formulae derived from clinical data. Fleischman D, Bicket AK, Stinnett SS, Berdahl JP, Jonas JB, Wang N, Fautsch MP, Allingham RR. Invest Ophthalmol Vis Sci. 2016;57:5625-5630.
8) Effect of intracranial pressure on the diameter of the optic nerve sheath. Watanabe A, Kinouchi H, Horiokoshi T, Uchida M, Ishigame K. J Neurosurg 2008 109(2): 255-8.
9) Optic nerve ultrasound for the detection of raised intracranial pressure. Rajajee V, Vanaman M, Fletcher JJ, Jacobs TL. Neurocrit Care 2011;15(3):506-15.
10) Sonographic assessment of the optic nerve sheath in idiopathic intracranial hypertension. Bauerle J, Nedelmann M. J Neurol 2011; 258(11):2014-9.
11) Measurement of Optic Nerve Sheath Diameter: Differences between Methods? A Pilot Study. Giger-Tobler C, Eisenack J, Holzmann D, Pangalu A, Sturm V, Killer HE, Landau K, Jaggi GP. Klin Monbl Augenheilkd. 2015 Apr;232(4):467-70
We read with great interest the article of Gokhale et al [1] on their retrospective study of metformin use and risk of age-related macular degeneration (AMD) in individuals with type 2 diabetes mellitus (T2DM). In this study Gokhale and colleagues used data derived from IQVIA Medical Research Data (IMRD-UK), formerly known as The Health Improvement Network (THIN), and found no change in AMD risk in those taking metformin.
An issue with this study is the quality of the GP coding and data on AMD. The authors cite a validation study of THIN data [2] but this study only validated cases identified as having AMD. There was no validation of the quality of data on the absence of AMD. So, the confirmation of positives was high (confirmed AMD cases quoted as 97%) but the false negative rate, is unknown. Also, the validation was by an ophthalmologist reviewing all the GP data, not using recognised diagnostic criteria or a grading scheme for AMD. Furthermore, the authors included a code for “drusen” into their AMD group which was not a code included in the validation study by Vassilev et al [2]. It is likely that this code includes patients with common physiological drusen and not an AMD diagnosis.
We have previously performed a systematic review and meta-analysis [3] of five studies [4–8] on the relationship between metformin use and AMD, which we have now updated to include Gokhale et al [1] and Jiang et al [9]. Including their data, we found a beneficial odds ratio of...
We read with great interest the article of Gokhale et al [1] on their retrospective study of metformin use and risk of age-related macular degeneration (AMD) in individuals with type 2 diabetes mellitus (T2DM). In this study Gokhale and colleagues used data derived from IQVIA Medical Research Data (IMRD-UK), formerly known as The Health Improvement Network (THIN), and found no change in AMD risk in those taking metformin.
An issue with this study is the quality of the GP coding and data on AMD. The authors cite a validation study of THIN data [2] but this study only validated cases identified as having AMD. There was no validation of the quality of data on the absence of AMD. So, the confirmation of positives was high (confirmed AMD cases quoted as 97%) but the false negative rate, is unknown. Also, the validation was by an ophthalmologist reviewing all the GP data, not using recognised diagnostic criteria or a grading scheme for AMD. Furthermore, the authors included a code for “drusen” into their AMD group which was not a code included in the validation study by Vassilev et al [2]. It is likely that this code includes patients with common physiological drusen and not an AMD diagnosis.
We have previously performed a systematic review and meta-analysis [3] of five studies [4–8] on the relationship between metformin use and AMD, which we have now updated to include Gokhale et al [1] and Jiang et al [9]. Including their data, we found a beneficial odds ratio of metformin use for “any AMD” remained (OR 0.75, 95% CI 0.54-0.97, I2=98.5%). This information should be interpreted with caution due to the high heterogeneity between studies including racial differences. We agree that further studies into the potential benefit of metformin for AMD are certainly warranted, including population-based datasets with accurate AMD diagnoses and prospective clinical trials.
Sincerely
References:
1. Gokhale KM, Adderley NJ, Subramanian A, et al. Metformin and risk of age-related macular degeneration in individuals with type 2 diabetes: a retrospective cohort study. British Journal of Ophthalmology Published Online First: 3 February 2022. doi:10.1136/bjophthalmol-2021-319641
2. Vassilev ZP, Ruigómez A, Soriano-Gabarró M, et al. Diabetes, Cardiovascular Morbidity, and Risk of Age-Related Macular Degeneration in a Primary Care Population. Invest Ophthalmol Vis Sci 2015;56:1585–92. doi:10.1167/iovs.14-16271
3. Romdhoniyyah DF, Harding SP, Cheyne CP, et al. Metformin, A Potential Role in Age-Related Macular Degeneration: A Systematic Review and Meta-Analysis. Ophthalmol Ther 2021;10:245–60. doi:10.1007/s40123-021-00344-3
4. Brown EE, Ball JD, Chen Z, et al. The Common Antidiabetic Drug Metformin Reduces Odds of Developing Age-Related Macular Degeneration. Invest Ophthalmol Vis Sci 2019;60:1470–7. doi:10.1167/iovs.18-26422
5. Stewart JM, Lamy R, Wu F, et al. Relationship between Oral Metformin Use and Age-Related Macular Degeneration. Oph Retina 2020;0. doi:10.1016/j.oret.2020.06.003
6. Blitzer AL, Ham SA, Colby KA, et al. Association of Metformin Use With Age-Related Macular Degeneration: A Case-Control Study. JAMA Ophthalmology Published Online First: 21 January 2021. doi:10.1001/jamaophthalmol.2020.6331
7. Chen Y-Y, Shen Y-C, Lai Y-J, et al. Association between Metformin and a Lower Risk of Age-Related Macular Degeneration in Patients with Type 2 Diabetes. Journal of Ophthalmology. 2019. doi:10.1155/2019/1649156
8. Lee H, Jeon H-L, Park SJ, et al. Effect of Statins, Metformin, Angiotensin-Converting Enzyme Inhibitors, and Angiotensin II Receptor Blockers on Age-Related Macular Degeneration. Yonsei Med J 2019;60:679–86. doi:10.3349/ymj.2019.60.7.679
9. Jiang J, Chen Y, Zhang H, et al. Association between metformin use and the risk of age-related macular degeneration in patients with type 2 diabetes: a retrospective study. BMJ Open 2022;12:e054420. doi:10.1136/bmjopen-2021-054420
Author: Dewi Fathin Romdhoniyyah (1), Nicholas AV Beare (1,2)
(1) Department of Eye and Vision Science, Institute of Life Course and Medical Sciences, University of Liverpool, Liverpool, UK
(2) St. Pauls Eye Unit, Liverpool University Hospitals NHS Foundation Trust, Liverpool, UK
Mauschitz et al. (1) conducted a meta-analysis to investigate the association of systemic medications with age-related macular degeneration (AMD) in the general population. A pooled odds ratios (95% confidence intervals [CIs]) of lipid-lowering drugs (LLD) and antidiabetic drugs for any AMD were 0.85 (0.79 to 0.91) and 0.78 (0.66 to 0.91), respectively. In contrast, late AMD was not significantly associated with systemic medications. There is an information that antidiabetics, lipid-lowering agents, and antioxidants could theoretically be repurposed for AMD treatment (2). I present information regarding the effect of antidiabetic medications on the risk of AMD.
Blitzer et al. (3) conducted a case-control study and metformin use was significantly associated with reduced odds of AMD, presenting dose dependent manner. But metformin did not have an effect of protecting diabetic retinopathy. In contrast, Gokhale et al. (4) conducted a retrospective cohort study to evaluate the effect of metformin on the risk reduction of AMD. The adjusted hazard ratio (95% CI) of patients prescribed metformin (with or without other antidiabetic medications) against those prescribed any other antidiabetic medication only for AMD was 1.02 (0.92 to 1.12). Vergroesen et al. (5) conducted a cohort study and a lower risk of AMD was not observed in patients with metformin, but other diabetes medication was significantly associated with a lower risk of AMD.
Mauschitz et al. (1) conducted a meta-analysis to investigate the association of systemic medications with age-related macular degeneration (AMD) in the general population. A pooled odds ratios (95% confidence intervals [CIs]) of lipid-lowering drugs (LLD) and antidiabetic drugs for any AMD were 0.85 (0.79 to 0.91) and 0.78 (0.66 to 0.91), respectively. In contrast, late AMD was not significantly associated with systemic medications. There is an information that antidiabetics, lipid-lowering agents, and antioxidants could theoretically be repurposed for AMD treatment (2). I present information regarding the effect of antidiabetic medications on the risk of AMD.
Blitzer et al. (3) conducted a case-control study and metformin use was significantly associated with reduced odds of AMD, presenting dose dependent manner. But metformin did not have an effect of protecting diabetic retinopathy. In contrast, Gokhale et al. (4) conducted a retrospective cohort study to evaluate the effect of metformin on the risk reduction of AMD. The adjusted hazard ratio (95% CI) of patients prescribed metformin (with or without other antidiabetic medications) against those prescribed any other antidiabetic medication only for AMD was 1.02 (0.92 to 1.12). Vergroesen et al. (5) conducted a cohort study and a lower risk of AMD was not observed in patients with metformin, but other diabetes medication was significantly associated with a lower risk of AMD.
Anyway, clinical trials are needed to specify the inconsistent relationship between antidiabetic medications and the risk reduction of AMD.
References
1. Mauschitz MM, Verzijden T, Schuster AK, et al. Association of lipid-lowering drugs and antidiabetic drugs with age-related macular degeneration: a meta-analysis in Europeans. Br J Ophthalmol 2022 doi: 10.1136/bjo-2022-321985
2. Nadeem U, Xie B, Xie EF, et al. Using advanced bioinformatics tools to identify novel therapeutic candidates for age-related macular degeneration. Transl Vis Sci Technol 2022;11(8):10.
3. Blitzer AL, Ham SA, Colby KA, Skondra D. Association of metformin use with age-related macular degeneration: A case-control study. JAMA Ophthalmol 2021;139(3):302-309.
4. Gokhale KM, Adderley NJ, Subramanian A, et al. Metformin and risk of age-related macular degeneration in individuals with type 2 diabetes: a retrospective cohort study. Br J Ophthalmol 2022 doi: 10.1136/bjophthalmol-2021-319641
5. Vergroesen JE, Thee EF, Ahmadizar F, et al. Association of diabetes medication with open-angle glaucoma, age-related macular degeneration, and cataract in the Rotterdam Study. JAMA Ophthalmol 2022;140(7):674-681.
The paper advises that the population inspected was predominately of white background and is looking to find ways of expanding its knowledge of non-white ethnicity within the sphere of retina testing. Within the following paper : Ethnicity and Type 2 diabetes in the UK by
L. M. Goff; it states that the prevalence of Type 2 diabetes within the non-white community is particularly high. a quote from this paper:
"Among minority ethnic communities, the prevalence is alarmingly high, approximately three to five times higher than in the white British population. "
Which brings me to my response: All UK Type 2 diabetics are offered eye screening during which the retina is photographed every year. These digital photographs are examined by medical staff looking for vein bleeding and are held by the NHS. Given the hign incidence of Type 2 diabetes in non-white citizens a very large number of these records will be available and so allow a useful extension to the work done by Professor Rudnicka.
26th September 2023
Dear Editor,
Show MoreWe read with great interest the study conducted by Yu X et al.1 comparing the efficacy of augmented surgical doses of surgery and Botulinum Toxin A injection for Acute acquired concomitant esotropia (AACE).
AACE has been on the rise with the advent of digital education for children, smartphones and change in lifestyles for both adults and children and hence this work is of particular interest to us.
We wish to report outcomes from our unpublished series of acquired esotropia. We retrospectively analyzed 29 patients of AACE, over a 17 month period between April 2022 and September 2023. As per protocol, we used surgical doses suggested by standard tables and did not use augmentation. The mean angle of deviation was 43.09 9.32 PD at 6m and 46.31 9.8 PD at 33cm preoperatively. The mean dose response without augmentation we achieved was 3.12 0.62 PD/mm and we achieved surgical success in 28 patients. The post operative final angles of deviation were 3.33 5.81 PD at 6m and 4.05-6.64 PD at 33cm at the last follow up. We used similar criteria of surgical success as Yu X et al.
Kim et al also report successful surgical outcomes in their subset of AACE patients using standard doses from Park’s tables.3
Augmented surgery has also been done by either increasing the amount of recession or resection and has resulted in good motor and sensory outcomes4,5
Yu et al recommend augmenting their surgical dose by...
Dear Editor, we read with interest the study of Hilely and coworkers, describing a new condition which they referred to as pachyvitelliform maculopathy. Their study clearly demonstrates the association between pachychoroid features and adult vitelliform lesions (AVLs).1 Two previous reports by our teams may stregthen their hypothesis of a relationship between the two conditions. In cuticular drusen, we have shown that vitelliform detachments occur significantly more often in eyes with a thick choroid, and we suggested that the choroidal vasculature could play a role in the occurrence of macular detachments in patients with cuticular drusen, leading to accumulation of photreceptors debris and deposits.2 More recently, we report a series of 49 eyes with hyperreflective vertical lines diagnosed on B-scans of spectral-domain optical coherence tomography. Twenty-four eyes presented with AVLs related to adult vitelliform dystrophy or pattern dystrophy. We were surprised that, in 14 cases out of 24, signs of pachychoroid were present. We suggested that further studies were needed to better understand this relationship.3 So we fully agree in that the pachychoroid syndrome may interfere with the metabolism of the retinal pigment epithelium and the phagocytosis process, leading to accumulation of photoreceptors debris. We really thank Hilely and coworkers for their convincing step towards a better recognition of this curious association.
Salomon Y Cohen, A Gaudric, Sarah Mrej...
Show MoreWe read with considerable attention the manuscript by Hilely et al. entitled “Pachyvitelliform maculopathy: an optical coherence tomography analysis of a novel entity.”1 We would like to compliment the Authors on their great effort and excellent figures.
Show MoreHilely and associated introduced a novel clinical entity named pachyvitelliform maculopathy (PVM). It consisted of the association between acquired vitelliform lesion (AVL) and pachychoroid disease spectrum (PDS) features, including pachychoroid (choroidal thickness > 250 μm), pachyvessels (dilated Haller vessels), and inner choroid thinning. In detail, a yellowish hyperreflective lesion overlayed a thick choroid and pachyvessels. In contrast to other forms PDS,2 PVM displayed no subretinal (SRF) or intraretinal fluid (IRF) and neovascularization. Furthermore, cases of pachychoroid and drusen (medium, large, cuticular, pseudo reticular, and subretinal drusenoid deposits) were excluded. This condition was described in 60 years older subjects with electro-oculogram within normal range and with a negative genetic test, although performed in a minority of the cohort.
We would like to have the thoughts about the following issue that Hilely and colleagues ought to address. Although the Authors stated that this was the first description of PVM, previous papers discussed the aforementioned association between PDS and vitelliform lesions. In detail, Spaide described three cases (two monoliteral, and one bilateral) o...
We thank Dr. Carkeet for his comments on our paper,1 which is now over 15 years old.
As discussed with Dr. Carkeet in personal correspondence recently, the discrepancy between his results and ours occurred because we simplified the 1 exam/year and 3 exam/years conditions by linearly scaling the outputs from the 2 exam/year condition. We repeated the simulations under the conditions Dr. Carkeet has outlined, and we agree with the result. The simulations yield approximately the same time required to detect the various rates of change for 2 exams per year, and slightly different values for 1 and 3 exams per year. He has pointed out discrepancies in the 1 and 3 exam per year conditions which appear large only in extreme conditions and are not realistic in clinical practice, for example, detecting a -0.25 dB/y change with high variability, where we estimated 30 years and Dr. Carkeet estimated 18 years.
In the final analysis simulations are only simulations that can be made with conditions assumed to reflect reality. The precision with which these estimates is made can be low. Ultimately, the message in our paper was that it takes a long time to detect a small amount of change if visual field results are variable and the testing frequency is low.
Our paper has been used to inform guidelines from various organizations and is based on one of the key messages of the paper, i.e., that ruling out fast progression (worse -2 dB/y or worse) requires 6 visual...
Show MoreTo the Editor:
We thank Dr Velez-Montoya and colleagues for their interest in our study.1 We reported that there was an increase in the prevalence of endophthalmitis after vitrectomy in Japan and found that it was probably related to the face masks during the COVID period.2 Although the cause for the increase definitively determined, we need to report these findings to the ophthalmologic community to alert them of this possibility.
First, we address the indicated point, “the definition of postoperative endophthalmitis was not rigorous”. We used the definition of the Endophthalmitis Vitrectomy Study group.3 Although this definition is relatively old, many subsequent studies have used it, and it has the advantage that our findings could be compared to these other studies with the same definition.
They also stated that the latest studies have shown that the sclerotomies after a pars plana vitrectomy seal within 15 days after the surgery even after a suture-less closure. Thus, the site of the incision was unlikely the entry port for the infectious micro-organisms after that time. This is generally true but the cause of infectious endophthalmitis after vitrectomy is complex. Because the cause of infectious endophthalmitis is varied, it is not surprising that anything can happen with postoperative endophthalmitis. For example, it is possible for a patient to inadvertently touch the eye in the early postoperative period and cause the incision to open. Once...
Show MoreChauhan and co-workers [1] have provided Table 1, showing times taken to detect significant field progression with 80% power, based on a number of modelling parameters: frequency of examinations, rate of field progression, intrasession variability of field assessment. They have also provided Table 2 showing the number of annual eye examinations required to detect different total visual field changes, for different time periods, and for moderate variability. I have checked the calculations of Chauhan and co-workers, using Monte Carlo modelling, assuming a one-tailed significance value of 0.025. Of the 36 outcome values in Table 1, 33 are incorrect. Of the 12 outcome values in Table 2, 11 are incorrect.
Chauhan and co-workers have made 2 main errors in their calculations for Table 1. The first is in applying their estimates of power. The curves shown in Figure 2 (statistical power plotted against number of field examinations) are appropriate for the case of 2 field examinations per year, but Chauhan and co-workers appear to have incorrectly also used them for the cases of 1 examination per year and 3 examinations per year. Separate sets of curves should have been calculated for those conditions. The effect on Table 1 is that the time taken to detect a field change is incorrectly reported as being inversely proportional to the number of examinations per year. This anomalous relationship was commented on by Albert Alm in his 2008 Rapid Response, “Is a field every 4...
Show MoreDear Editor:
We read the paper on non-invasive intracranial pressure determination by Zhang et al(1) with great interest and hope. We fully agree that the search for non-invasive intracranial pressure (ICP) evaluations is of high importance and should be continued. The Bland-Altman plot showing the difference between predicted and intracranially measured pressure looks very impressive. There are, however, still a few points and limits we would like to address concerning the anatomy of the optic nerve, the optic canal, and the basic concept the authors used.
Cerebrospinal fluid (CSF) from the intracranial subarachnoid spaces and the subarachnoid space of the optic nerve (SAS -ON) communicate via the optic canal. Using three-dimensional reconstruction of the optic canal in normal tension glaucoma (NTG) patients, this was found to be narrower than in an age-related cohort of normals,(2) thus questioning the patency of the CSF pathway between the pituitary cistern and the SAS-ON. Further, optic canal dimensions in a normal population are quite variable amongst individuals, and even between orbits within the same individual.(3) These facts largely influence the results the authors present. Further, studies in patients with NTG and patients with elevated ICP (such as patients with idiopathic intracranial hypertension) were shown to have developed an optic nerve sheath compartment syndrome. In such cases, the CSF dynamics between the intracranial CSF and the CSF in...
Show MoreWe read with great interest the article of Gokhale et al [1] on their retrospective study of metformin use and risk of age-related macular degeneration (AMD) in individuals with type 2 diabetes mellitus (T2DM). In this study Gokhale and colleagues used data derived from IQVIA Medical Research Data (IMRD-UK), formerly known as The Health Improvement Network (THIN), and found no change in AMD risk in those taking metformin.
An issue with this study is the quality of the GP coding and data on AMD. The authors cite a validation study of THIN data [2] but this study only validated cases identified as having AMD. There was no validation of the quality of data on the absence of AMD. So, the confirmation of positives was high (confirmed AMD cases quoted as 97%) but the false negative rate, is unknown. Also, the validation was by an ophthalmologist reviewing all the GP data, not using recognised diagnostic criteria or a grading scheme for AMD. Furthermore, the authors included a code for “drusen” into their AMD group which was not a code included in the validation study by Vassilev et al [2]. It is likely that this code includes patients with common physiological drusen and not an AMD diagnosis.
We have previously performed a systematic review and meta-analysis [3] of five studies [4–8] on the relationship between metformin use and AMD, which we have now updated to include Gokhale et al [1] and Jiang et al [9]. Including their data, we found a beneficial odds ratio of...
Show MoreMauschitz et al. (1) conducted a meta-analysis to investigate the association of systemic medications with age-related macular degeneration (AMD) in the general population. A pooled odds ratios (95% confidence intervals [CIs]) of lipid-lowering drugs (LLD) and antidiabetic drugs for any AMD were 0.85 (0.79 to 0.91) and 0.78 (0.66 to 0.91), respectively. In contrast, late AMD was not significantly associated with systemic medications. There is an information that antidiabetics, lipid-lowering agents, and antioxidants could theoretically be repurposed for AMD treatment (2). I present information regarding the effect of antidiabetic medications on the risk of AMD.
Blitzer et al. (3) conducted a case-control study and metformin use was significantly associated with reduced odds of AMD, presenting dose dependent manner. But metformin did not have an effect of protecting diabetic retinopathy. In contrast, Gokhale et al. (4) conducted a retrospective cohort study to evaluate the effect of metformin on the risk reduction of AMD. The adjusted hazard ratio (95% CI) of patients prescribed metformin (with or without other antidiabetic medications) against those prescribed any other antidiabetic medication only for AMD was 1.02 (0.92 to 1.12). Vergroesen et al. (5) conducted a cohort study and a lower risk of AMD was not observed in patients with metformin, but other diabetes medication was significantly associated with a lower risk of AMD.
Anyway, clinical trials are nee...
Show MoreThe paper advises that the population inspected was predominately of white background and is looking to find ways of expanding its knowledge of non-white ethnicity within the sphere of retina testing. Within the following paper : Ethnicity and Type 2 diabetes in the UK by
L. M. Goff; it states that the prevalence of Type 2 diabetes within the non-white community is particularly high. a quote from this paper:
"Among minority ethnic communities, the prevalence is alarmingly high, approximately three to five times higher than in the white British population. "
Which brings me to my response: All UK Type 2 diabetics are offered eye screening during which the retina is photographed every year. These digital photographs are examined by medical staff looking for vein bleeding and are held by the NHS. Given the hign incidence of Type 2 diabetes in non-white citizens a very large number of these records will be available and so allow a useful extension to the work done by Professor Rudnicka.
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