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Hypertensive Retinopathy
- 1. HYPERTENSIVE RETINOPATHY Reeta Karki B Optom, 2nd year 1
- 2. INTRODUCTION • Hypertension, also known as high blood pressure, is a long-term medical condition in which the blood pressure in the arteries is persistently elevated. High blood pressure usually does not cause symptoms. It is, however, a major risk factor for stroke, coronary artery disease, heart failure. • HTN affects the eye causing 3 types of ocular damage: – Retinopathy – Choroidopathy – Optic neuropathy • It represents ophthalmic findings of end-organ damage. 2
- 3. • In United States, – HTN , affects > 65 million Americans, – 25% of all adults – 60% of > 60 years are hypertensive • Nepal: 34% of elderly persons affected • Nearly 1% of hypertensive patients develop malignant hypertension • Men are affected more than women until age 50 when women have a higher prevalence Sharma SS et al. Prevalence of Hypertension, Obesity, Diabetes and Metabolic syndrome in Nepal. Int J Hypertens. 2011; 2011: 821971 3
- 4. • In the Beaver Dam Eye Study, which evaluated hypertensive patients without coexisting vascular diseases, the incidence of hypertensive retinopathy was about 15%. – 8% showed retinopathy, – 13% showed arteriolar narrowing, and – 2% showed arteriovenous nicking. • Diagnosing systemic hypertension from ophthalmic findings on examination was only 47–53% 4
- 5. • Relationship of hypertensive vascular changes with arteriosclerotic vascular disease. • It is complex and related to: 1. Duration of HTN 2. Severity of dyslipidemia 3. Smoking history 4. Age of patient 5
- 6. • Average time required to develop retinopathy was 6.73 yrs • Significantly higher in >50 yrs hypertensive patient • Higher in those with duration of HTN more than 5 yrs Mondal RN, Matin MA, Rani M, Hossain ZM, Shaha AC, et al. (2017) Prevalence and Risk Factors of Hypertensive Retinopathy in Hypertensive Patients. J Hypertens 6: 241. doi:10.4172/2167-1095.1000241 6
- 7. • The major risk for arteriosclerotic hypertensive retinopathy is the duration of elevated BP. • The major risk factor for malignant hypertension is the amount of BP elevation over normal. • Ocular changes in malignant hypertension can be – Disc edema – Choroidal infarction, and – Retinopathy. • Changes from chronic hypertension are more subtle, affecting primarily the retinal vasculature. 7
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- 10. Few Anatomical Considerations • Retinal arteries are histologically arterioles with 100 μm caliber, with no internal lamina or muscular coat. • Retinal arterioles & capillaries exhibit autoregulatory mechanism and tight junction to maintain blood-ocular barrier. • The resistance of flow is equivalent to fourth power of luminal diameter. • Features of retinal arterioles – Lumen – 8 to 15 μm – Media – 1 to 2 layer of smooth muscle cells – Adventitia - poorly developed 10
- 11. • Features of retinal arteries – Diameter of major branches -100 μm – Intima – single layer endothelial cells with no internal elastic lamina – Media – 5 to 7 layers of smooth muscle cells near optic disc, 2-3 layers in equator, 1-2 in periphery – Adventitia - thin 11
- 12. • Features of choroidal arteries – Diameter – 20 to 90 μm – Intima – endothelium, internal elastic lamina – Media – single layer of smooth muscles – Adventitia • Features of choroidal arterioles – Intima – internal elastic lamina absent – Media – layer of smooth muscle discontinuous – Adventitia – very less connective tissue 12
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- 14. Pathogenesis 1. Vasospasm • Vasospasm of retinal arterioles occur in young patients, & affected by pre-existing involutional sclerosis in older one. • Vasospasm of choroidal vessels & peripapillary choroid> ischaemia> HTN choroidopathy & HTN optic neuropathy. 2. Arteriosclerotic changes 3. Increased vascular permeability 4. Raised intracranial pressure 14
- 15. 15
- 16. Clinical features • Benign or chronic HTN retinopathy • Malignant HTN retinopathy 16
- 17. Benign or Chronic HTN Retinopathy 1. HTN with involutionary sclerosis • Comprise augmented arteriosclerotic retinopathy 2. Chronic HTN with compensatory arteriolar sclerosis • Albuminuric or renal retinopathy 17
- 18. Fundus changes in HTN retinopathy 1. Generalized arterial narrowing a. Vasoconstrictive phase: Due to diffuse vasospasm characterised by increased in retinal arteriolar tone. b. Sclerotic phase: Cause due to hypoplasia of tunica media, hyaline degeneration & characterised by increased arteriolar narrowing with tortuosity. 18
- 19. 2. Focal arteriolar narrowing: seen within ½ disc diameter of its margin zone. 3. Arteriovenous nicking • Salu’s sign : deflection of vein at arteriovenous crossings • Bonnet sign: banking of vein distal to AV crossing • Gunn sign : tapering of veins on either side of crossings. 19
- 20. 20 • SALUS SIGN
- 21. 4. Arteriolar Reflex Changes • Bright and thin, linear blood reflex seen because of blood column in arteriole, as vessel wall is transparent. • More diffuse and less bright reflex due to thickening of vessel wall, representing grade I & II HTN retinopathy • Copper wiring, reddish brown reflex due to progressive sclerosis and hyalinization, sign of grade III. • Silver wiring, opaque-white reflex due to continued sclerosis, seen in grade IV HTN retinopathy. 21
- 22. 22 Retinal arterioles appear orange or yellow instead of red (copper wiring), If become occluded (silver wiring)
- 23. 5. Superficial retinal haemorrhages • Due to disruption of capillaries in RNFL layer. • Disappear in 3-5 weeks. 23
- 24. 6.Hard Exudates • Lipid deposits in OPL of retina due to leaky capillaries • Appear as yellowish waxy spots with sharp margins. • Disappear in 3-6 weeks. 24
- 25. 7. Cotton wool spots • Fluffy white lesions, are the infarcts of RNFL layer. • Termed as soft exudates caused by capillary obliterations in severe HTN retinopathy. 25
- 26. Malignant hypertensive retinopathy • Acute HTN Retinopathy 1. Marked arteriolar narrowing due to spasm of arteriolar wall. 2. Superficial retinal haemorrhages in posterior pole 3. Focal intraretinal periarteriolar transudates due to deposition of macromolecules lead to breakdown of blood retinal barrier following dilatation of arterioles. 4. Cotton wool spot more marked. 5. Microaneurysms, shunt vessels & collaterals 26
- 27. • Acute hypertensive choroidopathy 1. Acute focal retinal pigment epitheliopathy, due to ischaemic change in choriocapillaries characterised by focal white spots. 2. Elschnig’s spot formed due to clumping & atrophy of infarcted pigment epithelium. They are small black spots surrounded by yellow halos. 3. Siegrist streaks formed due to fibrinoid necrosis. 4. Serous neurosensory retinal detachment due to accumulation of fluid beneath retina. 5. Manifest as exudative bullous retinal detachment with shifting subretinal fluid. 27
- 28. 3. Acute hypertensive optic neuropathy • Disc edema and haemorrhages on disc & peripallary retina. • Disc pallor 28
- 29. KEITH & WAGENER STAGING OF HTN RETINOPATHY 29
- 30. 30
- 31. MODIFIED SCHEIE CLASSIFICATION 31 STAGING OF RETINOPATHY CHANGES GRADE 0 NO CHANGES GRADE 1 BARELY DETECTABLE ARTERIAL NARROWING GRADE 2 OBVIOUS ARTERIAL NARROWING WITH FOCAL IRREGULARITIES GRADE 3 GRADE 2 PLUS RETINAL HAEMORRHAGES & EXUDATES GRADE 4 GRADE 3 PLUS DISC SWELLING
- 32. STAGING OF LIGHT REFLEX CHANGES GRADE 0 NORMAL GRADE 1 BROADENING OF LIGHT REFLEX WITH MINIMAL AV COMPRESSION GRADE 2 LIGHT REFLEX CHANGES & AV CROSSINGS CHANGES MORE PROMINENT GRADE 3 COPPER WIRE APPEARANCE & MORE PROMINENT AV COMPRESSION GRADE 4 SILVER WIRE APPEARANCE & SEVERE AV CROSSING CHANGES 32
- 34. Ocular Complications of Hypertension Branch retinal vein occlusion Central vein occlusion 34
- 35. Central retinal artery occlusion Branch artery occlusion Ocular Complications of Hypertension 35
- 36. Differential Diagnosis 1. High altitude retinopathy 2. Diabetic retinopathy 3. Radiation retinopathy 4. Retinal vein occlusion 36
- 37. Treatment and Outcome • Diagnosis of malignant hypertensive crisis represents a medical emergency. • Untreated mortality rate is 50% at 2 months and 90% at 1 year. • Treatment of malignant hypertensive retinopathy, choroidopathy, and optic neuropathy consists of lowering blood pressure in a controlled fashion to a level that minimizes end-organ damage 37
- 38. • Too rapid decline can lead to ischemia of the optic nerve head, brain, and other vital organs • Medications used to treat hypertensive emergencies include sodium nitroprusside, nitroglycerin, calcium channel blockers, beta blockers, and angiotensin-converting enzyme inhibitors 38
- 39. Lifestyle modification • Reducing weight, alcohol consumption, salt intake • Increased activity level is recommended • Reducing stress • Adopting Dietary Approach to Stop Hypertension (DASH) • Increase in calcium and potassium intake 39
- 40. Summary • Understanding hypertension and its ocular sequela is important. • Its direct effects on the retinal vessels may indicate the severity and chronicity of hypertension in patients. • Hypertensive retinopathy predicts CHD in patient independent of blood pressure and other risk factor. • Counseling patients to control their blood pressure optimally will benefit not only the overall management of their ocular conditions but more importantly protect them from life-threatening cardiovascular and cerebrovascular conditions. 40
- 41. References • American Academy of Ophthalmology. Section 12- Vitreous and Retina • Kanski JJ. Clinical Ophthalmology-A Systemic Approach. 9th ed. ELSEVIER • Yanoff M, Duker JD. Ophthalmology. 3rd edition • Comprehensive Ophthalmology, Ak Khurana 41
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Editor's Notes
- Hypertension is the most common medical condition Most important risk factor for condition results in significant morbidity and mortality Ocular manifestation has wide spread clinical spectrum, but may be subtle or nonexistent in patient with well controlled HTN May lead to direct effect in blood vessels, contribute to development and exacerbation of other retinal vasculopathies
- usually asymptomatic ; smoking_vasoconstricton d/t CO2 chronicity, duration-Increase in atherosclerosis younger pt with acute HTN more common older pt more atherosclerosis, rigid arterial wall
- (3 month, 30 yrs)
- The general architecture and cellular composition of blood vessels are same throughout the cardiovascular system.Certain features of the vasculature vary with and reflect distinct functional requirements at different locations (see below). To withstand the pulsatile flow and higher blood pressures in arteries, arterial walls are generally thicker than the walls of veins. Arterial wall thickness gradually diminishes as the vessels become smaller, but the ratio of wall thickness to lumen diameter becomes greater. The basic constituents of the walls of blood vessels are endothelial cells and smooth muscle cells, and extracellular matrix (ECM), including elastin, collagen, and glycosoaminoglycans. The three concentric layers—intima, media, and adventitia—are most clearly defined in the larger vessels, particularly arteries ( Fig. 11-1 ). In normal arteries, the intima consists of a single layer of endothelial cells with minimal underlying subendothelial connective tissue. It is separated from the media by a dense elastic membrane called the internal elastic lamina. The smooth muscle cell layers of the media near the vessel lumen receive oxygen and nutrients by direct diffusion from the vessel lumen, facilitated by holes in the internal elastic membrane. However, diffusion from the lumen is inadequate for the outer portions of the media in large and medium-sized vessels, therefore these areas are nourished by small arterioles arising from outside the vessel (called vasa vasorum, literally "vessels of the vessels") coursing into the outer one half to two thirds of the media. The outer limit of the media of most arteries is a well-defined external elastic lamina. External to the media is the adventitia, consisting of connective tissue with nerve fibers and the vasa vasorum. Based on their size and structural features, arteries are divided into three types: (1) large or elastic arteries, including the aorta, its large branches (particularly the innominate, subclavian,common carotid, and iliac), and pulmonary arteries; (2) medium-sized or muscular arteries, comprising other Figure 11-1 The vascular wall. A, Graphic representation of the cross section of a small muscular artery (e.g., renal or coronary artery). B, Photomicrograph of histologic section containinga portion of an artery (A) and adjacent vein (V). Elastic membranes are stained black (internal elastic membrane of artery highlighted by arrow). Because it is exposed to higher pressures,the artery has a thicker wall that maintains an open, round lumen, even when blood is absent. Moreover, the elastin of the artery is more organized than in the corresponding vein. In contrast, the vein has a larger, but collapsed, lumen, and the elastin in its wall is diffusely distributed. (B, Courtesy of Mark Flomenbaum, M.D., Ph.D., Office of the Chief Medical histology: large aterty:Tunica media: This is the thickest of the three layers. The smooth muscle cells are arranged in a spiral around the long axis of the vessel. They secrete elastin in the form of sheets, or lamellae, which are fenestrated to facilitate diffusion. The number of lamellae increase with age (few at birth, 40-70 in adult) and with hypertension. These lamellae, and the large size of the media, are the most striking histological feature of elastic arteries. In addition to elastin, the smooth muscle cells of the media secrete reticular and fine collagen fibers and proteoglycans (all not identifiable). No fibroblasts are present. medium arteries no sharp dividing line between elastic (large) and muscular (medium) arteries; in areas of transition, arteries may appear as intermediates between the two types. Medium arteries have less elastic tissue than large arteries, the predominant constituent of the tunica media is smooth muscle small ateries/arterioles:<0.5mm size in diameter; general construction of small arteries is very similar to that of muscular arteries. The media is still muscular and has up to 8-10 layers of smooth muscle cells. This number is reduced as the arteries get smaller, the smallest arterioles have 1-2 layers of smooth muscle cells. The adventitia becomes thinner and the external elastic membrane disappears. The intima becomes smaller and the internal elastic membrane also eventually disappears. However, it persist much longer than the external, and it is not uncommon to see very small arteries which still have an internal elastic membrane. Small arteries also maintain their shape, and tend to be round or oval. histology veins:classified as large, medium and small, and the sizes blend into one another with no sharp demarcations. Although the same layers (intima, media and adventitia) are present, they are often not as well defined as in arteries. A big difference between arteries and veins is the thickness of their walls and the relative amount of muscle tissue (media). In comparably sized vessels, arteries have thicker walls and a much larger media. In veins, the adventitia is larger than the media. Because of these features, veins do not retain their shape. They often appear floppy in sections, and the lumen may not be patent. Veins are frequently of an irregular shape. Veins also have less elastic tissue than do arteries. Even in larger veins, the internal elastic membrane may be poorly developed or absent.
- Diabetic retinopathy Collagen vascular diseases Bilateral central retinal vein obstruction High-altitude retinopathy
- Pt with family hx,other CAD should be counseled
- Chatterjee S et al. Hypertension and Eye: changing perspective. Journal of Human Hypertension (2002) 16, 667-675