This document discusses hypertensive retinopathy, which refers to retinal vascular changes caused by high blood pressure. It notes that the prevalence of hypertensive retinopathy is approximately 15% among hypertensive patients without other vascular diseases. The key signs include arteriolar narrowing, arteriovenous nicking, and cotton wool spots. The pathogenesis involves initial vasoconstriction, then exudation and fluid leakage due to damaged blood vessels, and finally arteriolar sclerosis. Hypertensive choroidopathy and optic neuropathy can also occur in severe untreated cases and are characterized by lesions such as Elsching spots. Strict blood pressure control and regular eye screening are important for treatment and prevention of further vision loss

1. Hypertensive Retinopathy
Sumit Singh Maharjan

2. INTRODUCTION
The overall prevalence of hypertension was 20.5 % and pre-
hypertension was 46.6%.
Prevalence and Associated Factors of Hypertension among Adults in Rural Nepal: A Community Based Study.
Chataut j et al,
Kathmandu univ med J, 2015

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 Beaver Dam 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
Eye is the only place in the body where the vessels can be directly
observed

5. • First described in 1859 as ‘albuminuric retinitis’ by Liebreich
• Angiospastic retinopathy, Hypertensive neuroretinopathy and
Hypertensive retinopathy

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

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

8. 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

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

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

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

12. 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

13. 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

14. 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)

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

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

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

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

19. ARTERIOLAR NARROWING
Ischaemia

20. VASCULAR LEAKAGE
Loss of endothelial cells or necrosis of muscle wall

21. 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

22. ARTERIOLOSCLEROSIS
Salus sign

23. ARTERIOLOSCLEROSIS
Gunn’s sign

24. ARTERIOLOSCLEROSIS
Bonnet’s sign

25. CLASSIFICATION

28. GRADE I

29. GRADE II

30. GRADE III

31. GRADE IV

32. ASSOCIATIONS
CRVO BRVO

33. ASSOCIATIONS
CRAO BRAO

34. DIFFERENTIAL DIAGNOSIS
Htn Retinopathy Diabetic Retinopathy

35. DIFFERENTIAL DIAGNOSIS
Hypertensive Retinopathy Retinal Venous Obstruction

36. DIFFERENTIAL DIAGNOSIS
Hypertensive retinopathy High altitudnal retinopathy

37. DIFFERENTIAL DIAGNOSIS
Hypertensive Retinopathy Radiation retinopathy

38. HYPERTENSIVE CHOROIDOPATHY

39. 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

40. 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

41. 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

42. 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

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

44. ELSCHING SPOT

45. 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 halos
ELSCHING’S SPOT

46. SIEGRIST STREAK

47. SIEGRIST STREAK

48. HYPERTENSIVE OPTIC NEUROPATHY

49. HYPERTENSIVE OPTIC NEUROPATHY

50. 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

51. 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

52. 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

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

55. 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

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

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

58. 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

59. 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
• 6th ed. ELSEVIER; 2008

60. THANK YOU