Diabetic Retinopathy: The Essentials

Diabetic Retinopathy—The Essentials. Gloria Wu. New York: Lippincott, pages, RRP $ Reviewed by: ERICA FLETCHER.
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Administered intravitreally; corticosteroid used in the treatment of diabetic macular edema. Administered intravitreally; monoclonal antibody that can help to reduce diabetic macular edema and neovascularization of the disc or retina. This involves directing a high-focused beam of light energy to create a coagulative response in the target tissue.

In nonproliferative diabetic retinopathy NPDR , laser photocoagulation is indicated in the treatment of clinically significant macular edema. This procedure can be used in PDR in cases of long-standing vitreous hemorrhage where visualization of the status of the posterior pole is too difficult , tractional retinal detachment, and combined tractional and rhegmatogenous retinal detachment.

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When laser photocoagulation in PDR is precluded in the presence of an opaque media, such as in cases of cataracts or vitreous hemorrhage, cryotherapy may be applied instead. See Treatment and Medication for more detail. Growth hormone appears to play a causative role in the development and progression of diabetic retinopathy. Diabetic retinopathy has been shown to be reversible in women who had postpartum hemorrhagic necrosis of the pituitary gland Sheehan syndrome. This led to the controversial practice of pituitary ablation to treat or prevent diabetic retinopathy in the s.

This technique has since been abandoned because of numerous systemic complications and the discovery of the effectiveness of laser treatment. It should be noted that diabetic retinopathy has been reported in parients with hypopituitarism as well. The variety of hematologic abnormalities seen in diabetes, such as increased erythrocyte aggregation, decreased red blood cell deformability, increased platelet aggregation, and adhesion, predispose the patient to sluggish circulation, endothelial damage, and focal capillary occlusion.

This leads to retinal ischemia, which, in turn, contributes to the development of diabetic retinopathy. Fundamentally, diabetes mellitus DM causes abnormal glucose metabolism as a result of decreased levels or activity of insulin.

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Increased levels of blood glucose are thought to have a structural and physiologic effect on retinal capillaries causing them to be both functionally and anatomically incompetent. A persistent increase in blood glucose levels shunts excess glucose into the aldose reductase pathway in certain tissues, which converts sugars into alcohol eg, glucose into sorbitol, galactose to dulcitol.

9781605476629 - Diabetic Retinopathy: The Essentials by Wu

Intramural pericytes of retinal capillaries seem to be affected by this increased level of sorbitol, eventually leading to the loss of their primary function ie, autoregulation of retinal capillaries. This results in weakness and eventual saccular outpouching of capillary walls. These microaneurysms are the earliest detectable signs of DM retinopathy.

See the image below. Using nailfold video capillaroscopy, a high prevalence of capillary changes is detected in patients with diabetes, particularly those with retinal damage. This reflects a generalized microvessel involvement in both type 1 and type 2 diabetes. Ruptured microaneurysms result in retinal hemorrhages either superficially flame-shaped hemorrhages or in deeper layers of the retina blot and dot hemorrhages. Increased permeability of these vessels results in leakage of fluid and proteinaceous material, which clinically appears as retinal thickening and exudates.

If the swelling and exudation involve the macula, a diminution in central vision may be experienced. Macular edema is the most common cause of vision loss in patients with nonproliferative diabetic retinopathy NPDR.

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However, it is not exclusively seen in patients with NPDR; it may also complicate cases of proliferative diabetic retinopathy. Another theory to explain the development of macular edema focuses on the increased levels of diacylglycerol from the shunting of excess glucose. This is thought to activate protein kinase C, which, in turn, affects retinal blood dynamics, especially permeability and flow, leading to fluid leakage and retinal thickening.

As the disease progresses, eventual closure of the retinal capillaries occurs, leading to hypoxia. Infarction of the nerve fiber layer leads to the formation of cotton-wool spots, with associated stasis in axoplasmic flow. More extensive retinal hypoxia triggers compensatory mechanisms in the eye to provide enough oxygen to tissues. Venous caliber abnormalities, such as venous beading, loops, and dilation, signify increasing hypoxia and almost always are seen bordering the areas of capillary nonperfusion.

Intraretinal microvascular abnormalities represent either new vessel growth or remodeling of preexisting vessels through endothelial cell proliferation within the retinal tissues to act as shunts through areas of nonperfusion. Further increases in retinal ischemia trigger the production of vasoproliferative factors that stimulate new vessel formation. The extracellular matrix is broken down first by proteases, and new vessels arising mainly from the retinal venules penetrate the internal limiting membrane and form capillary networks between the inner surface of the retina and the posterior hyaloid face.

See the images below. Neovascularization is most commonly observed at the borders of perfused and nonperfused retina and most commonly occurs along the vascular arcades and at the optic nerve head. The new vessels break through and grow along the surface of the retina and into the scaffold of the posterior hyaloid face. By themselves, these vessels rarely cause visual compromise, but they are fragile and highly permeable. These delicate vessels are disrupted easily by vitreous traction, which leads to hemorrhage into the vitreous cavity or the preretinal space.

These new blood vessels initially are associated with a small amount of fibroglial tissue formation. However, as the density of the neovascular frond increases, so does the degree of fibrous tissue formation. In later stages, the vessels may regress, leaving only networks of avascular fibrous tissue adherent to both the retina and the posterior hyaloid face.

As the vitreous contracts, it may exert tractional forces on the retina via these fibroglial connections. Traction may cause retinal edema, retinal heterotropia, and both tractional retinal detachments and retinal tear formation with subsequent detachment. In patients with type I diabetes , no clinically significant retinopathy can be seen in the first 5 years after the initial diagnosis of diabetes is made.

In patients with type II diabetes , the incidence of diabetic retinopathy increases with the disease duration. Systemic hypertension, in the setting of diabetic nephropathy, correlates well with the presence of retinopathy.

Diabetic retinopathy the essentials download

Independently, hypertension also may complicate diabetes in that it may result in hypertensive retinal vascular changes superimposed on the preexisting diabetic retinopathy, further compromising retinal blood flow. Proper management of hyperlipidemia elevated serum lipids may result in less retinal vessel leakage and hard exudate formation, but the reason behind this is unclear.

Pregnant women with proliferative diabetic retinopathy do poorly without treatment, but those who have had prior panretinal photocoagulation remain stable throughout pregnancy. A study by Toda et al found that among pregnant women with diabetic retinopathy, those who showed progression of the eye disorder tended to have a longer duration of diabetes, to have had diabetic retinopathy prior to pregnancy, and to have higher blood pressure in the second trimester.

For more information, see Diabetes Mellitus and Pregnancy. Of those who know they have diabetes, only half receive appropriate eye care. Thus, it is not surprising that diabetic retinopathy is the leading cause of new blindness in persons aged years in the United States.

Diabetic Retinopathy: The Essentials

Approximately , Americans have proliferative diabetic retinopathy, with an annual incidence of 65, Approximately , persons have clinically significant macular edema, with an annual incidence of 75, An increased risk of diabetic retinopathy appears to exist in patients of Native American, Hispanic, and African American heritage. The images are hopelessly inadequate, small, dark, and difficult or impossible to read, as well as being fairly frequently mislabeled.

The ones online are slightly better but not remotely of high quality. She used standard photo 2A for cotton-wool spots when it doesn't show any. Clearly no one did fact checking or proof-reading on this text, apparently including the author.

Whoever claims to have edited this work deserves to find new employment and this text makes me reluctant to purchase anything from Wolters Kluwer. I know this review sounds venomous but this book is beyond pitiful. Seemingly this was a resume builder or supposed practice enhancer but it is not of value to anyone trying to learn about diabetic retinopathy.

Great text however the photo quality is terrible. The lack of clarity and the constant under exposure renders the retinal images virtually useless. The on line version of the book is no better. I intended to use this as a supplemental text for optometry students as they see patients. Obviously I will have to look elsewhere.


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Wu is a well respected clinician and expert on diabetic eye disease whose retina fellowship training was at Harvard Medical School. She is a seasoned physician who distills her vast experience into the hands of the reader. This is her third book and I think it's even better than her first two. It is clearly written in a manner that will be helpful to all eye care professionals as well those in general medicine and endocrinology. It's said that "you can't judge a book by its cover" but I can attest that the carefully chosen and gorgeous panoply of high quality images inside do reflect its beautiful cover and these alone would make owning this gem of a book worthwhile.

Wu gives the reader so much more. She provides an excellent background about diabetic retinopathy, and then clearly, concisely yet comprehensively, and clinically relevantly describes the ophthalmic evaluation of the patient and appropriate tests, and then discusses treatments of different categories of diabetic retinopathy in the most up-to-date manner. The algorithms used in the book are clear and of great value. The book is timely in its ability to capture very recent therapeutic advances that are significantly changing how eye care professional practice.

Its breadth will appeal to a wide readership, and its depth will reward those seeking salient details-- even general diabetic medical issues are well covered. Additionally, the book uniquely provides clinically useful information regarding informed consent, guidelines for nurses and medical assistants, medical equipment and supplies, and diabetic recipes that the author developed. What makes Biblio different?

Sign In Register Help Cart 0. Search Results Results 1 of Book has minor flaw, like bent or scratched cover. We work every day but Sunday. Standard delivery takes business days. The Essentials Gloria Wu. Ergodebooks , Texas, United States Seller rating: Used book in very good condition.

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