Intraretinal Microvascular Abnormalities

Aiello LP, Gardner TW, King GL, et al. Diabetic retinopathy. Diabetes Care 1998; 21: 143-56

Angulo P. Nonalcoholic fatty liver disease. N Engl J Med 2002; 346: 1221-31

Archer AG, Watkins PJ, Thomas PK, Sharma AK, Payan J. The natural history of acute painful diabetic neuropathy. J Neurol Neurosurg Psychiatr 1983; 46: 491-9

Arkkila PE, Kantola IM, Viikari JS, et al. Dupuytren's disease in type 1 diabetic patients: a five-year prospective study. Clin Exp Rheumatol 1996; 14: 59-65

Barnett AH, Dodson PM. Hypertension and Diabetes. London: Science Press Ltd, 1990

Bell DS. Diabetic cardiomyopathy. A unique entity or complication of coronary artery disease? Diabetes Care 1995; 18: 708-14

Bommer J. Attaining long-term survival when treating diabetic patients with ESRD by hemodialysis. Adv Ren Replace Ther 2001; 8: 13-21

British Multicentre Study Group. Photocoagulation for -proliferative diabetic retinopathy: a randomised controlled clinical trial using the zenon arc. Diabetologia 1984; 26: 109-15

Chauhan A, Foote J, Petch MC, Schofield PM. Hyperinsu-linemia, coronary artery disease and syndrome X. J Am Coll Cardiol 1994; 23: 364-8

Donnelly R, Emslie-Smith AM, Gardner ID, Morris AD. ABC of arterial and venous disease: vascular complications of diabetes. Br Med J 2000; 320: 1062-6

Drury PL. Hypertension. Baillierès Clin Endocrinol Metab 1988; 2: 375-9

Dyck PJ, Thomas PK, Asbury AK, et al. Diabetic Neuropathy. Philadelphia: WB Saunders, 1987

Early Treatment of Diabetic Retinopathy Study Research Group. Photocoagulation for diabetic macular oedema. Arch Ophthalmol 1985; 103: 1796-806

Edmonds ME. The diabetic foot: pathophysiology and treatment. Clin Endocrinol Metab 1993; 15: 889-916

Eldor R, Raz I, Ben Yehuda A, Boulton AJM. New and experimental approaches to treatment of diabetic foot ulcers: a comprehensive review of emerging treatment strategies. Diabet Med 2004; 21: 1161-73

Estacio RO, Schrier RW. Diabetic nephropathy: pathogene-sis, diagnosis, and prevention of progression. Adv Intern Med 2001; 46: 359-408

Ewing DJ, Campbell IW, Clarke BF. The natural history of diabetic autonomic neuropathy. Q J Med 1980; 193: 95-108

Ferris FL 3rd, Davis MD, Aiello LM. Treatment of diabetic retinopathy. N Engl J Med 1999; 341: 667-78

Finne P, Reunanen A, Stenman S, et al. Incidence of endstage renal disease in patients with Type 1 diabetes. JAMA 2005; 294: 1782-7

Greene DA, Lattimer SA, Sima AAF. Sorbitol, phospho-inositides and sodium-potassium ATPase in the pathogenesis of diabetic complications. N Engl J Med 1987; 316: 599-606

Haffner SM. Epidemiology of insulin resistance and its relation to coronary artery disease. Am J Cardiol 1999; 84: 11J-14J

Ho T, Smiddy WE, Flynn HW Jr. Vitrectomy in the management of diabetic eye disease. Surv Ophthalmol 1993; 37: 190-202

Hutchinson A, McIntosh A, Peters J, et al. Effectiveness of screening and monitoring tests for diabetic retinopathy - a systematic review. Diabet Med 2000; 17: 495-506

Jacobson SH, Fryd D, Sutherland DER, Kjellstrand CM. Treatment of the diabetic patient with end-stage renal failure. Diabetes Metab Rev 1988; 4: 191-200

Jelinek JE. The skin in diabetes. Diabetic Med 1993; 10: 210-13

Kohner EM, Porta M, eds. Screening for Diabetic Retinopa-thy in Europe: A Field Guidebook. Copenhagen: WHO Regional Office for Europe, 1992

Kohner EM. Diabetic retinopathy. Br Med J 1993; 307: 1195-9

Lewis EJ, Hunsicker LG, Pain RP, Rohde RD. The effect of angiotensin-converting enzyme inhibition on diabetic nephropathy. N Engl J Med 1993; 329: 1456-65

Malmberg K. Prospective randomised study of intensive insulin treatment on long term survival after acute myocar-dial infarction in patients with diabetes mellitus. GIGAMI (Diabetes Mellitus, Insulin Glucose Infusion in Acute Myocardial Infarction) Study Group. Br Med J 1997; 314: 1512-15

McCulloch DK, Young RJ, Prescott RJ, Clarke BF. The natural history of impotence in diabetic men. Diabetologia 1984; 26: 437-40

Mead A, Burnett S, Davey C. Diabetic retinal screening in the UK. J R Soc Med 2001; 94: 127-9

Mogensen CE, ed. Microalbuminuria predicts clinical pro-teinuria and early mortality in maturity-onset diabetes. N Engl J Med 1984; 310: 356-60

Mogensen CE, ed. The Kidney and Hypertension in Diabetes Mellitus. Boston: Martinus Nijhoff Publishing, 1988

Mogensen CE, Cooper ME. Diabetic renal disease: from recent studies to improved clinical practice. Diabet Med 2004; 21:4-17

Passadakis P, Oreopoulos D. Peritoneal dialysis in diabetic patients. Adv Ren Replace Ther 2001; 8: 22-41

Perez MI, Kohn SR. Cutaneous manifestations of diabetes mellitus. J Am Acad Dermatol 1994; 30: 519-31

Ramsey SD, Newton K, Blough D, et al. Incidence, outcomes, and cost of foot ulcers in patients with diabetes. Diabetes Care 1999; 22: 382-7

Reaven GM. Role of insulin resistance in human disease. Diabetes 1988; 37: 1595-607

Scobie IN, MacCuish AC, Barrie T, et al. Serious retinopathy in a diabetic clinic: prevalence and therapeutic implications. Lancet 1981; 2: 520-1

Shapiro LM. A prospective study of heart disease in diabetes mellitus. Q J Med 1984; 209: 55-68

Spruce MC, Potter J, Coppini DV. The pathogenesis of painful diabetic neuropathy: a review. Diabet Med 2003; 20: 88-98

Stern M. Natural history of macrovascular disease in type 2 diabetes. Role of insulin resistance. Diabetes Care 1999; 22 (Suppl 3): c2-5

Taylor KG, ed. Diabetes and the Heart. Tunbridge Wells: Castle House Publications, 1987

UK Prospective Diabetes Study Group. Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38. Br Med J 1998; 317: 703-13

UK Prospective Diabetes Study Group. Efficacy of atenolol and captopril in reducing risk of macrovascular and microvascular complications in type 2 diabetes; UKPDS 39. Br Med J 1998; 317: 713-20

Vinik Al, Park TS, Stansberry KB, Pittenger GL. Diabetic neuropathies. Diabetologia 2000; 43: 957-73

Watkins PJ. The diabetic foot. Br Med J 2003; 326: 977-9

Young MJ, Boulton AJM, MacLeod AF, et al. A multicentre study of the prevalence of diabetic peripheral neuropathy in the United Kingdom hospital clinic population. Diabetologia 1993; 35: 150-4

Young RJ, Clarke BF. Pain relief in diabetic neuropathy: the effectiveness of imipramine and related drugs. Diabetic Med 1985; 2: 363-6

Young RJ, Ewing DJ, Clarke BF. Chronic remitting painful diabetic polyneuropathy. Diabetes Care 1988; 11: 34-40

Yusuf S, Sleight P, Pogue J, et al. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, oncardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med 2000; 342: 145-53

Normal Fundus Diabetes Fundus

Figure 81 Normal fundus of the eye. Appreciation of the fundal abnormalities seen in diabetes must be based on a sound knowledge of the normal appearance

Optic Atrophy Fundus Picture

Figure 82 Optic atrophy in the DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy and deafness) syndrome, a rare condition that is usually diagnosed when type 1 diabetes mellitus (DM) presents in childhood. The inheritance is autosomal recessive and the diabetes insipidus tends to develop after the diagnosis of type 1 DM

Figure 81 Normal fundus of the eye. Appreciation of the fundal abnormalities seen in diabetes must be based on a sound knowledge of the normal appearance

Figure 82 Optic atrophy in the DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy and deafness) syndrome, a rare condition that is usually diagnosed when type 1 diabetes mellitus (DM) presents in childhood. The inheritance is autosomal recessive and the diabetes insipidus tends to develop after the diagnosis of type 1 DM

Childhood Diabetic Retinopathy

Figure 83 Background diabetic retinopathy with occasional scattered microaneurysms and dot hemorrhages

Intraretinal Microaneurysms Abnormality

Figure 84 Fluorescein angiogram of the same area as in Figure 83 reveals many more abnormalities than can be seen on the fundal photograph. Widespread microaneurysms appear as white dots

Figure 83 Background diabetic retinopathy with occasional scattered microaneurysms and dot hemorrhages

Figure 84 Fluorescein angiogram of the same area as in Figure 83 reveals many more abnormalities than can be seen on the fundal photograph. Widespread microaneurysms appear as white dots

Intraretinal Microvascular Abnormality

Figure 85 Severe background diabetic retinopathy includes venous changes, clusters and large blot hemorrhages, intraretinal microvascular abnormalities (IRMA), an early cottonwool spot and a generally ischemic appearance. This type of retinopathy is usually a prelude to proliferative change

Fluorescein Angiogram Eye

Figure 86 Fluorescein angiogram of the same area as in Figure 85 shows the blind ends of occluded small vessels, widespread capillary leakage and areas of non-perfusion

Figure 85 Severe background diabetic retinopathy includes venous changes, clusters and large blot hemorrhages, intraretinal microvascular abnormalities (IRMA), an early cottonwool spot and a generally ischemic appearance. This type of retinopathy is usually a prelude to proliferative change

Figure 86 Fluorescein angiogram of the same area as in Figure 85 shows the blind ends of occluded small vessels, widespread capillary leakage and areas of non-perfusion

Cotton Wool Exudate And Hard Exudate

Figure 87 Serious diabetic retinopathy with venous irregularities, blot hemorrhages, intraretinal microvascular abnormalities, large cottonwool spots and extensive areas of hard exudates

Intraretinal Microvascular Abnormalities

Figure 88 Serious gross peripheral proliferative diabetic retinopathy includes marked venous changes such as dilatation and beading

Figure 87 Serious diabetic retinopathy with venous irregularities, blot hemorrhages, intraretinal microvascular abnormalities, large cottonwool spots and extensive areas of hard exudates

Figure 88 Serious gross peripheral proliferative diabetic retinopathy includes marked venous changes such as dilatation and beading

Group Hard Exudate

Figure 89 Circinate exudative retinopathy. The two hard exudate rings (lateral to the macula) are true exudates due to leakage from abnormal vessels and are associated with retinal edema. When hard exudates and retinal edema affect the macular area, the fovea may become involved, which may threaten central vision. Laser photocoagulation helps to prevent such loss of vision

Figure 89 Circinate exudative retinopathy. The two hard exudate rings (lateral to the macula) are true exudates due to leakage from abnormal vessels and are associated with retinal edema. When hard exudates and retinal edema affect the macular area, the fovea may become involved, which may threaten central vision. Laser photocoagulation helps to prevent such loss of vision

Vitreous Abnormalitys
Figure 91 Triamcinolone has been inserted into the vitreous under topical anesthesia
Macula Hard Exudates Ring
Figure 90 This retinal photograph shows the picture of diabetic maculopathy with frequent hard exudates around the macula immediately prior to intravitreal triamcinolone therapy

Figure 92 The same retina as in Figure 90 at 3 months post intravitreal triamcinolone therapy. The changes are not dramatic, but there is an improvement with partial resolution of hard exudates around the macula. The role of intravitreal triamcinolone therapy has not been fully established; however, some retina specialists use it to treat diabetic macular edema which persists despite laser therapy. It is not a substitute for laser therapy and one recent study showed it had only a marginal benefit over the long term, while increasing the incidence of cataract and glaucoma

Leash Vessels Eye

Figure 94 Leashes of peripheral new vessels with associated hemorrhage. These lesions are amenable to laser photocoagulation

Figure 93 Extensive peripheral proliferative retinopathy with venous beading and blot hemorrhages. New vessels usually originate from a major vein and adopt a branching pattern. Proliferative retinopathy is the most common sight-threatening complication of type 1 diabetes mellitus (DM), with visual loss being due to breakage of vessels leading to preretinal or vitreous hemorrhage. It is always accompanied by other diabetic lesions and is treatable by laser photocoagulation. It is less common in type 2 DM (where exudative maculopathy is the most common cause of visual loss)

Figure 94 Leashes of peripheral new vessels with associated hemorrhage. These lesions are amenable to laser photocoagulation

New Vessels The Optic Disc

Figure 95 Fluorescein angiogram (a) and fundal photograph (b) of new vessels at the optic disc, which lead rapidly to visual loss. If hemorrhage has already occurred, then visual loss is imminent and urgent laser treatment is indicated. Fluorescein angiography reveals the gross leakage from the abnormal vessels

Figure 95 Fluorescein angiogram (a) and fundal photograph (b) of new vessels at the optic disc, which lead rapidly to visual loss. If hemorrhage has already occurred, then visual loss is imminent and urgent laser treatment is indicated. Fluorescein angiography reveals the gross leakage from the abnormal vessels

Gross Disc New Vessels
Figure 96 Vitreous hemorrhage has occurred despite extensive laser photocoagulation. The hemorrhage may clear but, if it fails to do so or recurrent hemorrhage ensues, visual loss is inevitable and vitreoretinal surgery may be indicated
Fluorescein Angiography Traction

Figure 98 In profoundly ischemic diabetic eyes, thromboneovascular glaucoma may occur with new vessel and fibrous tissue proliferation in the angle of the anterior chamber, which interferes with normal aqueous drainage. The condition is associated with rubeosis iridis (shown here) wherein new vessel growth occurs on the iris

Diabetic Retinopathy End Stage

Figure 97 End-stage diabetic retinopathy is characterized by gross distortion of the retina with extensive fibrous bands. Uncontrolled new vessels develop a fibrous tissue covering and expanding fibrous tissue tends to contract, causing retinal traction and detachment. The result is sudden and unexpected visual loss. The retinopathy shown here is untreatable

Figure 97 End-stage diabetic retinopathy is characterized by gross distortion of the retina with extensive fibrous bands. Uncontrolled new vessels develop a fibrous tissue covering and expanding fibrous tissue tends to contract, causing retinal traction and detachment. The result is sudden and unexpected visual loss. The retinopathy shown here is untreatable

Grid Laser Photocoagulation

Figure 99 A patient undergoing laser photocoagulation for diabetic retinopathy. A high-energy light beam is focused through a corneal contact lens onto the target area of the retina. Laser photocoagulation can be used to destroy specific targets (e.g. peripheral new vessels) or to perform panretinal photocoagulation

Figure 99 A patient undergoing laser photocoagulation for diabetic retinopathy. A high-energy light beam is focused through a corneal contact lens onto the target area of the retina. Laser photocoagulation can be used to destroy specific targets (e.g. peripheral new vessels) or to perform panretinal photocoagulation

Figure 98 In profoundly ischemic diabetic eyes, thromboneovascular glaucoma may occur with new vessel and fibrous tissue proliferation in the angle of the anterior chamber, which interferes with normal aqueous drainage. The condition is associated with rubeosis iridis (shown here) wherein new vessel growth occurs on the iris

Papillomacular Bundle

Figure 100 Panretinal laser photocoagulation. The entire retina is treated except for the macula and papillomacular bundle, which are essential for central vision. The rationale for using photocoagulation in proliferative retinopathy is that it destroys the ischemic areas of retina which produce vasoproliferative factors that stimulate new vessel growth. Panretinal photocoagulation may require 1500-2000 burns. The treatment is well tolerated and divided into several sessions, and regression of new vessels is usually seen within 3-4 weeks. Once treatment is effective, the results are long-lasting. In maculopathy, laser treatment is either focused on discrete lesions or uses a diffuse 'grid' treatment in cases of widespread capillary leakage and non-perfusion. However, treatment is less effective and the long-term outlook is not as good

Figure 100 Panretinal laser photocoagulation. The entire retina is treated except for the macula and papillomacular bundle, which are essential for central vision. The rationale for using photocoagulation in proliferative retinopathy is that it destroys the ischemic areas of retina which produce vasoproliferative factors that stimulate new vessel growth. Panretinal photocoagulation may require 1500-2000 burns. The treatment is well tolerated and divided into several sessions, and regression of new vessels is usually seen within 3-4 weeks. Once treatment is effective, the results are long-lasting. In maculopathy, laser treatment is either focused on discrete lesions or uses a diffuse 'grid' treatment in cases of widespread capillary leakage and non-perfusion. However, treatment is less effective and the long-term outlook is not as good

Non Alcoholic Steatohepatosis

Figure 101 Severe vitreous hemorrhage may lead to secondary retinal detachment. Although vitrectomy may be performed electively for severe vitreous hemorrhage alone, urgent surgery is required for operable retinal detachment. Vitreoretinal microsurgery requires a closed intraocular approach (shown here). An operating microscope allows precise intraocular manipulation to remove the vitreous and its contained hemorrhage, which is replaced with saline and followed by endolaser photocoagulation to prevent both further detachment and subsequent neovascularization

Indications for and urgency of referral to an ophthalmologist

Is there evidence of: Vitreous hemorrhage Neovascular glaucoma

Delicious Diabetic Recipes

Delicious Diabetic Recipes

This brilliant guide will teach you how to cook all those delicious recipes for people who have diabetes.

Get My Free Ebook


Responses

Post a comment