I’ve read some articles etc. about this stuff before, but I’ve never read ‘the textbook’. I have now. Well, I’ve read a textbook anyway. I am not super impressed by the book, and I decided to give it two stars on goodreads. Maybe it deserves three, it’s in that neighbourhood.
So what’s the book about? Here’s what they write in the introduction:
“In this book the fundamental approach is to describe the classification of diabetes, risk factors for diabetic retinopathy and lesions of diabetic retinopathy, and explain the significance of these lesions in terms of progression of the disease, recommended treatment and consequences for vision. Methods of screening for diabetic retinopathy and other retinal conditions that are more frequent in diabetes or have similar appearances to diabetic retinopathy are also discussed.”
They deal with main concepts and they provide a lot of examples and case histories along the way. As is always the case in books like these many of the case histories are really quite depressing – I was considering skipping them altogether at one point after a particularly ‘bad one’, but I decided to read those parts anyway; they make up a substantial part of the book.
As you might have inferred from the remarks above, diabetic retinopathy is diabetes-related eye disease. How many diabetics are impacted by this? A rather large number, it turns out (well, I already knew that and I’ve talked about it before, but…):
“Diabetic retinopathy is a leading cause of adult blindness in the US, reported by Fong et al. in 2004 to result in blindness for over 10,000 people with diabetes per year. Moss reported the 10-year incidence of blindness in the Wisconsin Epidemiological study of Diabetic Retinopathy to be 1.8%, 4.0% and 4.8% in the younger-onset, older-onset taking insulin, and older-onset not taking insulin groups, respectively. Respective 10-year rates of visual impairment were 9.4%, 37.2% and 23.9%. […] In the Wisconsin study, proliferative retinopathy occurred in 67% of people with type 1 diabetes for 35 or more years. One would therefore expect that two-thirds of people with type 1 diabetes would need laser treatment for proliferative diabetic retinopathy during their lifetime. […] In patients with type 2 diabetes, the rate of proliferative diabetic retinopathy is not as high but it is estimated that 1 in 3 patients with type 2 diabetes will develop sight-threatening diabetic retinopathy requiring laser during their lifetime. […] Despite major advances in treatment and early detection of diabetic eye disease, the ageing demographic and increased incidence of diabetes is resulting in greater numbers of diabetic visually impaired people in the population.” [my emphasis. Numbers differ across countries and there are a lot more numbers in the book, but these estimates provide some context; this is a complication that affects a huge number of diabetics.]
In the book they talk a lot about how you can use tiny (with sizes measured in microns!) and very short-lasting laser pulses to treat the damaged blood vessels in the eyes, and that stuff’s quite interesting. Equally interesting is the fact that people seem to be treating without really knowing exactly why the treatment works:
“The effectiveness of focal laser treatment may be due, in part, to the closure of leaky microaneurysms, but the specific mechanisms by which focal photocoagulation reduces macular oedema is not known. Studies have shown histopathological changes and biochemical changes,[19,20] which have been suggested as mechanisms for improvement in macular oedema although some investigators have suggested alternative mechanisms for clearance of the oedema such as the application of Starling’s law and improved oxygenation. […] the mechanism by which laser treatment improves the prognosis of sight-threatening diabetic retinopathy is ill-understood.”
A lot has happened when it comes to treatment over the last decades, as patients in the pre-laser era would often simply lose their vision because no good treatment options existed. A lot of people still do lose their vision to diabetes as mentioned above, but with the advent of laser treatments the prognosis has improved a lot. There are some adverse effects associated with these treatments, e.g. in the form of laser scars or scotomas and (paradoxical?) development of macular oedema afterwards (“McDonald showed that 43% of the treated eyes in his study developed increased macular oedema 6–10 weeks following laser treatment.”), and it doesn’t always work (“if there is ischaemia that involves the central fovea, laser treatment in isolation is unlikely to improve the vision.” “It is not uncommon to successfully treat one area of leakage and subsequently find leakage appearing in a completely different area around the fovea of the same eye.”). But it’s still a big step in the right direction. Laser therapy is however surgical management of tissue damage, and some people are of course hoping to develop pharmacological treatment options as well. In that context I should note that in a way it was fun to read a medical textbook written by people who know less about some aspects of the stuff I’m reading about than do people I’ve met personally (people like Toke Bek). Latanoprost is being evaluated in a clinical trial right now as a drug which might be used to slow the progression of diabetic retinopathy in diabetics, but they don’t talk about that at all in the ‘Future advances in the management of diabetic retinopathy’-chapter (however on the other hand you can’t really blame them for not including this stuff, as that idea postdates the book..).
It should be noted – and they do this repeatedly throughout the book – that the damage to the small blood vessels in the eyes and the subsequent retinal ischaemia/bleeding etc. leading to vision loss in diabetics is strongly linked to factors such as glycemic control and (systemic) blood pressure. This means that improvements in glycemic control and blood pressure management will, if they can be achieved, also translate into better outcomes along these dimensions over time. A factor pulling in the other direction (‘more blind people’) is the high number of current and future undiagnosed type two diabetics who’ll incur extensive tissue damage without knowing it before getting their diagnoses:
“In the UKPDS study it was observed that up to 50% of [type 2] patients had some detectable form of tissue damage at diagnosis, the majority of this being background diabetic retinopathy. […] Retinopathy is the commonest finding, with about 30% of all subjects newly diagnosed having detectable retinal lesions.”
This patient population poses some problems also because these people will by definition not be included in national screening programs. A related point they do not touch upon in the book is of course that non-compliant patients, the ones most likely to benefit from participation, would also be expected to be less likely than other patient groups to participate in screening programs; so even in places where you have national screening programs and so on you’ll likely still have some ‘theoretically preventable’/’excess’ diabetes-related blindness in the future. Perhaps I talk about screening programs as if I think they’re a good idea, but if that’s the case it’s because some forms of them are almost certainly pretty much a no-brainer – see e.g. this post. The book also spends a chapter on that stuff, unsurprisingly coming to the conclusion that screening is probably a good idea (there’s also consensus about which method of screening is best: “There is widespread agreement that digital photography is the best method of screening for sight-threatening DR.”). It’s worth noting in the context of the complication rates that it’s easier to spot eye damage than other types of tissue damage, and that this may provide part of the explanation for why this complication is so often found at diagnosis compared to other types of complications – here’s a relevant passage from the book:
“Retinopathy is often the easiest complication to detect because the smallest of lesions (microaneurysms) can be visualized long before any change to the subjective function of the eye would be apparent. Retinopathy tracks closely with nephropathy, and so careful screening of renal function needs to be carried out in those who have retinopathy and vice versa.”
The book has a lot more stuff, but I know that most readers probably aren’t too interested in this topic so I figured a rather limited coverage of the book would be preferable to most readers. One of multiple reasons why I did not give it a higher rating is that they repeat themselves quite a few times, covering the same stuff in multiple chapters. Unless you’re a diabetic there’s also no good reason why you should read the book as it is quite technical. Most diabetics will probably find it hard to read.