Hypertensive retinopathy consists of retinal vascular changes caused by elevated blood pressure. It progresses through vasoconstrictive, exudative, and sclerotic phases. Key features include arteriolar narrowing, AV nicking, hemorrhages, and cotton wool spots. Left untreated, malignant hypertension can lead to hypertensive choroidopathy characterized by Elsching spots and Siegrist streaks, as well as hypertensive optic neuropathy. Strict blood pressure control and regular screening can help prevent progression of hypertensive eye disease.

1. Hypertensive Retinopathy
Dr Md Afzal Mahfuzullah
MCPS,FCPS,Felow Vitreo-Retina
Assistant Professor(Vitreo-Retina)
Bangabandhu Sheikh Mujib Medical University

2. INTRODUCTION
Hypertensive retinopathy consist of a spectrum of retinal vascular
changes that are pathologically related to both transient & persistent
microvascular damage from elevated blood pressure

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.
The overall prevalence of retinopathy was 5.4%.
The prevalence rates of retinopathy among diabetic, impaired glucose regulation
and non-diabetic subjects were 21.6%, 13% and 3.5%, respectively.
Additionally, age, body mass index, triglyceride and total cholesterol were also
found to be significant independent risk indicators for the occurrence of
retinopathy in this population.
Prevalence and Associated Risk Indicators of Retinopathy in a Rural Bangladeshi Population With and Without Diabetes
Opthalmic Epidemiol 2013 Aug;20(4)

4. Eye is the only place in the body where the vessels can be directly observed

5. ETIOLOGY
• Race:
Blacks > Whites
Afro-Caribbeans > Europeans
But prevalence of retinopathy Afro-Caribbeans < Europeans

6. ETIOLOGY
• Sex:
Women > Men
• Smoking
Positive association

7. ETIOLOGY
• Genetic factors
The D (deletion) allele of the angio-tensin converting enzyme (ACE)
gene is an independent risk factor for the development of end-organ
damage
2.4 fold higher chance of retinopathy

8. ETIOLOGY
• Renal status:
persistent microalbuminuria - early end-organ damage including
retinopathy
• Cardiac status:
More common in concentric hypertrophy

9. ETIOLOGY
• Secondary hypertension:
Renal hypertension secondary to focal segmental sclerosis and
membranoproliferative glomerulonephritis -severe retinopathy
Pheochromocytoma-grade III or IV retinopathy

10. PATHOGENESIS
Phases:
Vasoconstrictive
Exudative
Sclerotic and its complications

11. VASO-CONSTRICTIVE PHASE
• Reversible stimulation of the vascular tone of muscular retinal
arteries as an autoregulatory mechanism
• Prolonged blood pressure elevation, definitive narrowing
(angiotensin II, vasopressin) of the vascular lumen at the
precapillary level occurs

12. VASO-CONSTRICTIVE PHASE
• Cotton wool spots (feature of inner retinal ischemia)
• Interruption of axonal orthograde and retrograde energy dependent
organelle transport in the ganglion cell axons, swollen interrupted
nerve

13. EXUDATIVE PHASE
Vascular endothelial necrosis or disruption (Disruption of the
blood–retinal barrier )
Transudation of plasma into the vessel wall, around pericytes and
arteriolar muscle cells
Retinal HGE of various shapes and locations
Edema and exudates (the macular region)

14. SCLEROTIC PHASE
• Fibrinoid necrosis or hyaline degeneration
• Hyperplasia of the vascular tunica media
• Arteriosclerosis
• Narrowing of arteries
• A-V crossing abnormalities

15. CLINICAL FEATURES
• Chronic hypertensive retinopathy
• Hypertensive choroidopathy
• Hypertensive optic neuropathy

16. RETINOPATHY
• Hypertensive retinopathy consists of spectrum of retinal vascular
changes that are pathologically related to microvascular damage
from elevated blood pressure

17. RETINOPATHY
KEY FEATURES
• Narrowing and irregularities of retinal arteries
• AV nicking
• Blot retinal hemorrhage
• Cotton wool spots

18. ARTERIOLAR NARROWING
Ischaemia

19. VASCULAR LEAKAGE
Loss of endothelial cells or necrosis 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. ARTERIOLOSCLEROSIS
Salus sign

22. ARTERIOLOSCLEROSIS
Gunn’s sign

23. ARTERIOLOSCLEROSIS
Bonnet’s sign

24. CLASSIFICATION

27. Arterial Narrowing & Stratening
Sclerosis may shorten or elongate retinal arterioles with the branches coming off at
right angles.
This change in length deflects the veins at the common sheath and changes the
course of the vein (Salus sign).

28. Extra vascular retinal lesions
Microaneuyrisms
Retinal hemorrhages -- Streak hemorrhages located in the nerve fiber layer
predominate over the blot hemorrhages located deeper in the outer
plexiform layer.
Cotton wool spots
Retinal and macular edema
Retinal lipid deposits macular star is the most predominant appearance,
and this appearance is due to the radially oriented nerve fiber layer of
Henle.

29. GRADE I

30. GRADE II

31. GRADE III

32. GRADE IV

33. ASSOCIATIONS
CRVO BRVO

34. ASSOCIATIONS
CRAO BRAO

35. DIFFERENTIAL DIAGNOSIS
Htn Retinopathy Diabetic Retinopathy

36. DIFFERENTIAL DIAGNOSIS
Hypertensive Retinopathy Retinal Venous Obstruction

37. DIFFERENTIAL DIAGNOSIS
Hypertensive retinopathy High altitudnal retinopathy

38. DIFFERENTIAL DIAGNOSIS
Hypertensive Retinopathy Radiation retinopathy

39. HYPERTENSIVE CHOROIDOPATHY

40. INTRODUCTION
• 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, dimunition of vision,
photopsia and headache

41. INTRODUCTION
• Seen typically in young patients with pliable vessels that are not yet
sclerotic from long-term hypertension
• Toxemia of pregnancy, renal disease, pheochromocytoma,essential
hypertension, and connective tissue diseases

42. PATHOGENESIS
• Greater effect on the choroidal circulation than on retinal circulation
• The retinal vessels – autoregulatory mechanisms transiently maintain
the vascular tone in response to sudden rise in BP

43. PATHOGENESIS
• The sympathetic nervous system - choroidal vasculature - constrict
in response to rise in BP
• Due to shorter distance and fewer branchings of the choroidal
arteries, systemic hypertension is transmitted more
effectively

44. HYPERTENSIVE CHOROIDOPATHY
• Characterised by:
Elsching spots
Siegrist streaks
Exudative retinal detachment

45. ELSCHING SPOT

46. PATHOGENESIS
• Choroid arteries 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 haloes
ELSCHING’S SPOT,Cont

47. SIEGRIST STREAK

48. SIEGRIST STREAK

49. HYPERTENSIVE OPTIC NEUROPATHY

50. HYPERTENSIVE OPTIC NEUROPATHY

51. 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 disc.

52. HYPERTENSIVE OPTIC NEUROPATHY
• Optic nerve head is susceptible to ischemia by virtue of its tightly
arranged nerve fibers within a nonexpandable intrascleral canal.
• Vasoconstriction of the posterior ciliary arteries: results from the
release of angiotensin II and other vasoconstricting agents.

53. PATHOGENESIS
Ischaemia of optic nerve head
Delay in the axoplasmic transport and a subsequent accumulation
of axonal components in the lamina scleralis region
plasma leakage and disruption of nerve fibers leading to
Subsequent gliosis

55. COURSE
• It rarely results in significant loss of vision
• Ongoing end-organ damage is more important than actual blood
pressure

56. TREATMENT
• Treatment of the underlying systemic condition can halt the
progression but arteriolar narrowing and AV nicking usually
are permanent.
• Hypertensive emergencies: sodium nitroprusside, nitroglycerin,
calcium channel blockers, beta blockers, and angiotensin-converting
enzyme inhibitors.
• Blood pressure should be lowered in a controlled fashion.

57. OUTCOME
Malignant hypertension if untreated,
Mortality rate is 50% at 2 months 90% at 1 year

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

59. 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:
• Strict control of Blood pressure and periodic screening

60. References
• Retina Ryan 5th edition
• American Academy of Ophthalmology. 2013-14; Section 12- Vitreous
and Retina
• Kanski JJ. Clinical Ophthalmology-A Systemic Approach
• Yanoff M, Duker JD. Ophthalmology. 4th edition

61. THANK YOU