hypertensive retinopathy Retina disease.pptx

Retina,
hypertension

1. Hypertensive Retinopathy Prof Dr. MOKHLESUR RAHMAN

2. I NTRODUCTION The overall prevalence of hypertension was 20.5 % and pre-hypertension was 46.6%.

3. Prevalence of Hypertensive retinopathy The incidence of hypertensive retinal changes is variable and often masked by the presence of other retinal vascular disease such as diabetes. In the Eye Study, which evaluated hypertensive patients without coexisting vascular diseases, the incidence of hypertensive retinopathy was about 15%; specifically, 8% showed retinopathy, 13% showed arteriolar narrowing, and 2% showed arteriovenous nicking.

4. Ocular manifestations E ye is the only place in the body where the vessels can be directly observed

5. ETIOLOGY

6. ETIOLOGY

7. ETIOLOGY

8. ETIOLOGY

9. ETIOLOGY

10. P ATHOGENESIS

11. V ASO-CONSTRICTIVE PHASE

12. V ASO-CONSTRICTIVE PHASE

13. E XUDATIVE PHASE V ascular endothelial necrosis or disruption ( Disruption of the blood–retinal barrier ) Transudation of plasma into the vessel wall , around pericytes and arteriolar muscle cells R etinal HGE of various shapes and locations E dema and exudates ( the macular region )

14. S CLEROTIC PHASE

15. CLINICAL F E ATURES

16. R E TINOPATHY H ypertensive retinopathy consists of spectrum of retinal vascular changes that are pathologically related to microvascular damage from elevated blood pressure

17. R E TINOPATHY

18. ARTERIOLAR NARROWING Ischaemia

19. V ASCULAR LEAKAGE L oss of endothelial cells or necro sis of muscle wall

20. ARTERIOLOSCLEROSIS (hardening of the arteries) Collagen deposition within the wall (like onion skin) Hypertrophy and hyperplasia of arteriolar smooth muscle Loss of vessel wall elasticity

21. A RTERIOLOSCLEROSIS Salus sign

22. A RTERIOLOSCLEROSIS Gunn’s sign

23. A RTERIOLOSCLEROSIS Bonnet’s sign

24. CLASSIFICATION

25. GRADE I

26. GRADE II

27. GRADE III

28. GRADE IV

29. ASSOCIATIONS CRVO BRVO

30. ASSOCIATIONS CRAO BRAO

31. DIFFERENTIAL DIAGNOSIS Htn Retinopathy D iabetic Retinopathy

32. DIFFERENTIAL DIAGNOSIS Hypertensive Retinopathy Retinal Venous Obstruction

33. DIFFERENTIAL DIAGNOSIS Hypertensive retinopathy H igh altitudnal retinopathy

34. DIFFERENTIAL DIAGNOSIS Hypertensive Retinopathy Radiation retinopathy

35. High-altitude retinopathy component of the altitude illness syndrome ( acute mountain sickness, pulmonary edema and cerebral edema ) occurs above 10 , 000 ft (3000 m) due to functional hypoxia resulting in hemorrhage through endothelial tight-junction leakage in the retinal vasculature (Fig. 320.15) d ifferentiated from hypertensive retinopathy in that marked retinal arteriolar and venular dilatation (Fig. 320.16, Wiedman’s classification) occurs in high-altitude retinopathy Other ocular aspects of high-altitude hypoxia include papilledema , vitreous hemorrhage, rod threshold elevation and increased light adaptation recovery time, paradoxical pupillary dilatation, and flickerfusion decrement

36. HYPERTENSIVE CHOROIDOPATHY

37. I NTRODUCTION Seen in Malignant hypertension in which the blood pressure is 200/140 mm Hg associated with ocular, cardiac, renal and cerebral involvement Visual disturbances : scotoma , diplopia , dim u n ition of vision, photopsia and headache

38. INTRODUCTION

39. PATHOGENESIS

40. PATHOGENESIS

41. HYPERTENSIVE CHOROIDOPATHY

42. E LSCHING SPOT

43. P A THOGENESIS C horoid a rteries and arterioles undergo fibrinoid necrosis due to vessel-wall damage from severe spastic narrowing This results in patchy nonperfused areas of the choriocapillaris The overlying RPE appears yellow (focal ischemic infarcts) in the acute phase and with time becomes irregularly pigmented with depigmented halos ELSCHING’S SPOT

44. S IEGRIST STREAK

45. S IEGRIST STREAK

46. HYPERTENSIVE OPTIC NEUROPATHY

47. HYPERTENSIVE OPTIC NEUROPATHY

48. HYPERTENSIVE OPTIC NEUROPATHY Some propose that it occurs secondary to encephalopathy Others believe that it occurs in the absence of the raised ICP and is secondary to the ischemic changes of the optic dis c

49. HYPERTENSIVE OPTIC NEUROPATHY O ptic nerve head is susceptible to ischemia by virtue of its tightly arranged nerve fibers within a nonexpandable intrascleral canal V asoconstriction of the posterior ciliary arteries : result s from the release of angiotensin II and other vasoconstricting agents

50. P ATHOGENESIS I schaemia of optic nerve head delay in the axoplasmic transport and a subsequent accumulation of axonal components in the lamina scleralis region p lasma leakage and disruption of nerve fibers leading to subsequent gliosi s

51. COURSE

52. TREATMENT

53. OUTCOME

54. n engl j med 351;22 www.nejm.org november 25, 2004

55. SUMMARY Retina is the only place where hypertensive vascular changes can be directly observed Pathogenesis: Vasoconstriction, exudation, arteriolosclerosis Manifestations: Retinopathy, choroidopathy, neuropathy Hallmark: AV changes and cotton wool spots Classification: S trict control of Blood pressure and periodic screening

56. It is important to keep in mind the age of the patient in considering these vascular changes, because it is virtually impossible to distinguish the difference between the early vascular changes of hypertension and arteriosclerotic changes due to the normal aging process

57. Fibrinoid necrosis occurs in retinal vessels only in severe hypertensive cases. Retinal edema, serous exudates, and focal bullous detachments are often present, and secondary exudative retinal detachments can result from severe choroidopathy. (Macroaneurysms and capillary microaneurysms may also develop, predominantly from the radial peripapillary capillaries in the nerve fiber layer, which gives the flame-shaped quality (Fig. 320.14).58,59 Cystoid macular edema and epiretinal membrane formation may follow

58. patho

59. patho

60. patho

61. patho

62. Autoregulation of B/s

63. References Retina Ryan 5 th edition A merican Academy of Ophthalmology. 201 3-14 ; Section 12- Vitreous and Retina Kanski JJ. Clinical Ophthalmology-A Systemic Approach . Yanoff M, Duker JD. Ophthalmology. 4 th edition 6 th ed. ELSEVIER; 2008

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