Dear Editor,

We read with great interest the report by Alwitry et al [1] on severe decompression retinopathy after medical treatment of acute angle closure. The authors have speculated that the mechanism of the ‘preretinal’ haemorrhage in this case was similar to the scattered ‘intraretinal’ haemorrhages seen in ocular decompression retinopathy. Although we agree with them that the haemorrhage was caused by sudden lowering of intraocular pressure (IOP), we believe that the exact pathophysiological mechanism, as well the clinical signs, in this case were different from the condition originally described by Fechtner et al [2].

It can be hypothesised that a pupillary block caused the volume of aqueous humor in the posterior chamber to increase markedly. The vitreous gel was therefore pushed toward the posterior pole. Following medical therapy the pupillary block was reversed and the aqueous humor moved rapidly through the pupil from the posterior chamber to the anterior chamber. This coupled with decreased aqueous production due to administration of aqueous suppressants allowed the vitreous body to move forward rapidly. This induced a rapid posterior vitreous detachment (PVD), disrupting small vessels on the retinal surface or optic disc, and resulted in the subhyaloid haemorrhage. In the present case the very short duration of raised IOP makes significant impairment of autoregulation of retinal vasculature unlikely and the absence of multiple intraretinal haemorrhages rules out a general compromise of mechanical stability of retinal capillaries. Obana et al [3] were the first to demonstrate a subhyaloid haemorrhage caused by PVD induced after laser iridectomy for primary angle-closure glaucoma and it should be distinguished from ocular decompression retinopathy.

This leads to an interesting conclusion that a sudden lowering of IOP may cause posterior segment bleeding by three different mechanisms. Ocular decompression retinopathy is caused by overwhelming of capacitance of retinal capillaries and results in multiple intraretinal haemorrhages. The second mechanism and clinical picture is similar to a central retinal vein occlusion [4,5]. A sudden change in hydrostatic equation between the posterior and anterior chambers, induces a rapid PVD and may result in subhyaloid haemorrhage, as in this case.

Figure 1 Three different mechanisms of posterior segment bleeding after sudden lowering of intraocular pressure

References

1. Alwitry A, Khan K, Rotchford A et al. Severe decompression retinopathy after medical treatment of acute primary angle closure. Br J Ophthalmol 2007;91:121

2. Fechtner RD, Minckler D, Weinreb RN et al. Complications of glaucoma surgery. Ocular decompression retinopathy. Arch Ophthalmol 1992;110:965-8

3. Obana A, Gohto Y, Ueda N, Miki T, Cho A, Suzuki Y. Retinal and subhyaloid hemorrhage as a complication of laser iridectomy for primary angle-closure glaucoma. Arch Ophthalmol. 2000 Oct;118:1449-51

4. Suzuki R, Nakayama M, Satoh N. Three types of retinal bleeding as a complication of hypotony after trabeculectomy. Ophthalmologica. 1999;213:135-8

5. Dev S, Herndon L, Shields MB. Retinal vein occlusion after trabeculectomy with mitomycin C. Am J Ophthalmol. 1996 Oct;122:574-5

In their paper "Repetitive tests of visual function improved visual acuity in young subjects" Otto and Michelson [1] assessed effects of practice on visual acuity, using the Freiburg Visual Acuity Test "FrACT" developed by one of us [2,3]. At first glance they seem to confirm our findings [4], which showed a marked increase of visual acuity after visual training, more than 0.1 logMAR. At closer inspection, discrepancies emerge: During the first 7 sessions, Otto and Michelson's found only a random variability. Then, suddenly, acuity improved in most subjects, and inter-subject variability decreased markedly. In contrast, we found a continuous improvement starting already during the first session (one session comprised 14 acuity test runs) [4]. When we provided feedback by displaying the correct orientation after the response, we found a marked additional step increase in performance already between the first and second session. (Otto and Michelson do not mention whether or not they employed feedback.) The shape of the time course has theoretical implications: A sudden increase of visual acuity like that reported by Otto and Michelson would suggest a "discovery effect" rather than a "fluency effect" [5].

Otto and Michelson's data on contrast sensitivity are also challenging to understand, not only because the authors used the terms contrast threshold and contrast sensitivity interchangeably (the one is the reciprocal of the other). Looking at figure 1B and supplementary figure 2B, we suspect that the stated effect size of 45% (derived only from the last data point in the graph) can be attributed to random fluctuations, given the non-monotonous change of average contrast sensitivity over sessions. Otto and Michelson seem to share our reservation, since they write in the Discussion "the progress was not consistent enough to show a significant percentage development in one direction". Hopefully, this number 45% will not stick with readers, who could miss the fact that the p values where not derived from the same comparisons as the effect size.

The reason why the learning curves of Otto and Michelson's subjects are different from those of Heinrich et al's subjects remains speculative. The methods appear to be similar. It is, however, unclear whether Otto and Michelson used feedback and whether or not they presented the optotypes separately or in rows. Furthermore, the participants underwent a practice scheme that included several different visual tasks, so it is difficult to attribute improvement of performance to any single task or combination of tasks. Clearly, future careful studies in this exciting field promise further insights and clinical applications.

References

1 Otto J, Michelson G. Repetitive tests of visual function improved visual acuity in young subjects. Br J Ophthalmol 2014;98:383-6. doi:10.1136/bjophthalmol-2013-304262

2 Bach M. The Freiburg Visual Acuity Test - Automatic measurement of visual acuity. Optom Vis Sci 1996;73:49-53.

3 Bach M. Homepage of the Freiburg Visual Acuity & Contrast Test ('FrACT'). 2009. http://michaelbach.de/fract.html

4 Heinrich SP, Krueger K, Bach M. The dynamics of practice effects in an optotype acuity task. Graefes Arch Clin Exp Ophthalmol 2011;249:1319 -26. doi:10.1007/s00417-011-1675-z

5 Kellman PJ, Garrigan P. Perceptual learning and human expertise. Phys Life Rev 2009;6:53-84. doi:10.1016/j.plrev.2008.12.001

Conflict of Interest:

None declared

Dear Editor,

In their article Doctors Agrawal and McKibbin evaluate the one-year frequency and the clinical outcome data of Putscher’s retinopathy through the British Ophthalmological Surveillance Unit. [1] All their 15 cases were visually symptomatic. Twelve cases were associated with trauma and 3 cases with acute pancreatitis. The authors conclude that the incidence of Purtsher’s retinopathy is low (0.24 cases per million population) in the United Kingdom, and that in half of the cases visual acuity improves by at least 2 Snellen lines in 6 months. The authors’ data, however, need careful interpretation. We investigated the clinical characteristics, histological features and prognostic significance of retinopathy of pancreatitis (Purtscher’s retinopathy associated with acute pancreatitis) in several studies. [2][3] We found that most of our cases were visually asymptomatic, since the patients were in severe or terminal status in intensive care units. We also found that retinopathy of pancreatitis was an indicator of multi-organ failure and lethal outcome. Our data suggest that pancreatitis associated Purtscher’s retinopathy is more common than reported by Doctors Agrawal and McKibbin, and that the visual outcome may be worse than found by the authors who used data reported by ophthalmologists. One may suppose that the reporting ophthalmologists might have seen only those cases which were associated with less severe systemic damage, and therefore the patients were able to realise their visual symptoms. It is probable that Purtscher’s retinopathy is more frequent than reported by the authors for the United Kingdom, and that the visual outcome is different from that indicated in their article, if all cases are considered.

Correspondence to: Gábor Holló, Department of Ophthalmology, Semmelweis University, Budapest; hg@szem1.sote.hu

The author has no commercial interest in any product mentioned in the article or the comment.

References

1.Agrawal A, McKibbin M. Purtscher’s retinopathy: epidemiology, clinical features and outcome. Br J Ophthalmol 2007;91:1456-1459.
2.Holló G, Bobek I. Clinicopathology of a case with retinopathy of pancreatitis. Acta Ophthalmol (Copenh) 1993;71:422-425.
3.Holló G, Tarjányi M, Varga M, et al. Retinopathy of pancreatitis indicates multiple-organ failure and poor prognosis in severe acute pancreatitis. Acta Ophthalmol (Copenh) 1994;72:114-117.

O'Day and colleagues describe in their recent paper the inadequate reporting of harm in randomized controlled trials of intra-vitreal therapies for diabetic macular oedema(O'Day et al., 2014). At first glance, the results are alarming. An average of only six recommendations of the 2004 CONSORT guidelines extension covering harms were met. Ophthalmologists are not alone in their inadequate reporting, however. Several other studies have found similar, and often worse examples of heterogenous and selective reporting of harm in RCTs in psychological medicine(Jonsson et al., 2014), asthma(Ntala et al., 2013) and cancer(Sivendran et al., 2014). Why, then, are we falling so far short of these internationally agreed standards, and who is to blame?

Some might argue that there are too many recommendations. The CONSORT guidelines have 25 points, of which one is harm reporting (with ten recommendations)(Schulz et al., 2010). Whilst most published RCTs do not report them all, many do report on half or more (interquartile range 5-7 for the ophthalmic studies cited)(O'Day et al., 2014). In any case, they remain "recommendations", not "requirements" In order to address this, the recommendations might be adapted to suggest full reporting be made publically available elsewhere to limit the length of published reports.

Perhaps the authors of the RCTs published are to blame? Could it be that they simply do not the data needed to fulfill the ten requirements? Whilst it is possible, and in some cases may highlight the need for investment in training, most authors could likely fulfill more of the ten recommendations than they currently do, for example the number of patients withdrawn due to an adverse event (only 36% in ophthalmic trials)(O'Day et al., 2014), essential data that most investigators surely can trace(Ioannidis JA and Lau J, 2001).

Finally, it might be argued that journal editors are to blame for failing to implement these standards. This may not be an option for all except editors of the minority of most desirable publications. Raising the bar too high may lead to authors taking their work elsewhere where they know it will be accepted.

How, then, to move forward? Like many "culture change" challenges faced in modern medicine, the adequate adoption of such standards requires a concerted effort by all parties involved in the research-publication pathway. John Kotter's 8-step change model provides some insights as to how, including establishing a sense of urgency by highlighting the harms associated with poor reporting, and forming powerful coalitions(Kotter, 1996). Most importantly, however, we as researchers must champion the improvement of reporting standards in our own work and demand this of our peers. Only then can we hope for change.

Ioannidis JA, and Lau J (2001). Completeness of safety reporting in randomized trials: An evaluation of 7 medical areas. JAMA 285, 437-443. Jonsson, U., Alaie, I., Parling, T., and Arnberg, F.K. (2014). Reporting of harms in randomized controlled trials of psychological interventions for mental and behavioral disorders: a review of current practice. Contemp. Clin. Trials 38, 1-8. Kotter, J.P. (1996). Leading Change (Harvard Business Press). Ntala, C., Birmpili, P., Worth, A., Anderson, N.H., and Sheikh, A. (2013). The quality of reporting of randomised controlled trials in asthma: a systematic review. Prim. Care Respir. J. J. Gen. Pract. Airw. Group 22, 417-424. O'Day, R., Walton, R., Blennerhassett, R., Gillies, M.C., and Barthelmes, D. (2014). Reporting of harms by randomised controlled trials in ophthalmology. Br. J. Ophthalmol. 98, 1003-1008. Schulz, K.F., Altman, D.G., and Moher, D. (2010). CONSORT 2010 Statement: Updated Guidelines for Reporting Parallel Group Randomized Trials. Ann. Intern. Med. 152, 726-732. Sivendran, S., Latif, A., McBride, R.B., Stensland, K.D., Wisnivesky, J., Haines, L., Oh, W.K., and Galsky, M.D. (2014). Adverse event reporting in cancer clinical trial publications. J. Clin. Oncol. Off. J. Am. Soc. Clin. Oncol. 32, 83-89.

Conflict of Interest:

None declared