This document summarizes hypertensive retinopathy, which occurs when retinal vessels are damaged due to elevated blood pressure. It discusses the types and clinical features of hypertensive retinopathy, including changes to retinal arteries and veins seen on examination. It also covers classifications of hypertensive retinopathy based on vessel changes and light reflexes. Risk factors, pathophysiology, and complications are described. Treatment involves controlling blood pressure through lifestyle changes and medication. Uncontrolled high blood pressure can lead to further eye and systemic damage.

1. BIPIN KOIRALA MASTERS’ OF OPTOMETRY HIMALAYAN EYE INSTITUTE
HYPERTENSIVE
RETINOPATHY

2. CONTENTS
 Introduction
 Types
 Clinical features
 Classifications
 Treatment

3.  Poorly controlled hypertension (HTN) affects
several systems such as the cardiovascular, renal,
cerebrovascular, and retina.
 The damage to these systems is known as target-
organ damage.

4. Hyper tension
 Systolic >> 140mm hg
 Diastolic >> 90 mm hg

7.  HTN affects the eye causing 3 types of ocular
damage:
1. Choroidopathy
2. Retinopathy
3. Optic neuropathy.

8.  Hypertensive retinopathy (HR) occurs when the
retinal vessels get damaged due to elevated blood
pressure
 The incidence of retinopathy is related to the
degree of severity and duration of HTN

9. Risk factors
 Essential Hypertension
 Women >>> Men
 Afro-Caribbean Races
 Genetic factors (Certain genotypes have increased
risk of hypertensive retinopathy)

10.  Positive family history of HTN and retinopathy
 The deletion of the allele of the angiotensin-
converting enzyme increases the risk
 Lifestyle (Smoking, Alcohol)
 Renal Dysfunction

13. Pathophysiology
 Retinal blood vessels have distinct features, which
differentiate them from other blood vessels
1. The absence of sympathetic nerve supply
2. Auto regulation of blood flow
3. Presence of blood-retinal barrier

14.  Thus, an increase in blood pressure (BP) is
transferred directly to the vessels which initially
constrict.
 However, a further increase in BP overcomes this
compensatory tone and damage to the muscle
layer and endothelium occurs.

15. 3 phases of HTN retinopathy
1. Vaso constrictive Phase
 In this phase, the local auto regulatory mechanisms
come into play.
 This causes vasospasm and retinal arteriole narrowing,
causing decrease in the arteriole to veins
 In older patients with arteriosclerosis, focal arteriolar
narrowing develops,

16. 2. Sclerotic Phase
 Persistent increase in BP causes certain changes in
vessel wall:
 Intima layer: Thickening
 Media layer: Hyperplasia
 Arteriolar wall: Hyaline degeneration
 This leads to a severe form of arteriolar narrowing,
arterio-venous (AV) crossing changes, and widening
of light reflex (silver and copper wiring).

17.  AV crossing changes occur when a thickened
arteriole crosses over a venule and subsequently
compresses it
 The vessels share a common adventitious sheath
at A-V crossing
 The vein, in turn, appears dilated and torturous
distal to the AV crossing.

18. 3. Exudative Phase
 Seen in patients with severely increased BP;
characterized by the disruption of the blood-retinal
barrier
 Leakage of blood and plasma
 Increased vascular permeability

19.  In this stage, retinal signs occur such as
1. Retinal hemorrhage (flame-shaped and dot blot),
2. Hard Exudate formation,
3. Retinal ischemia (cotton-wool spots).
4. Optic disc odema

20. Clinical features of HTN Retinopathy
 Arterial changes
1. Decrease in the arterio venous ratio to 1:3 ( the
normal ratio is 2:3).
2. Change in the arteriolar light reflex (light reflex
appears as copper and/or silver wiring)

22.  AV Crossing Changes
1. Salus’s sign: Deflection of retinal vein as it crosses the
arteriole.
2. Gunn’s sign: Tapering of the retinal vein on either
side of the AV crossing.
3. Bonnet’s sign: Banking of the retinal vein distal to the
AV crossing.

24. Bonnet signs actually involves a triad:
1. A-V nicking ( Gunn
sign)
2. Cotton wool spot
3. Splinter haemmorage

25. Retinal Changes
 Retinal hemorrhages:
1. Dot-blot hemorrhages: Bleeding
in the inner retinal layer
2. Flame shaped hemorrhage:
Bleeding is in the superficial
retinal layer

26.  Retinal exudates:
1. Hard exudates: Lipid deposits in the retina
2. Soft exudates: Cotton wool spots

27. Macular Changes
 Macular star formation due to deposition of hard
exudates around the macula.

28. Scheie grading
(Based on vessel changes)1953
1. Stage 0: No visible abnormalities
2. Stage 1: Diffuse Arteriolar narrowing
3. Stage 2: Stage 1 + Focal arteriolar constriction
4. Stage 3: Stage 2 + Retinal hemorrhage
5. Stage 4: Stage 3 + Hard exudates + retinal edema+ optic
disc swelling

30. Scheie Classification
(Based on light reflex from arteries)
1. Stage 0: Normal
2. Stage 1: Broadening of arteriolar light reflex
3. Stage 2: Stage 1 + AV crossing changes
4. Stage 3: Copper wiring of arterioles
5. Stage 4: Silver wiring of arterioles

33. Keith-Wagner- Barker Classification
1. Group 1: Slight constriction of retinal arterioles
2. Group 2: Group 1 + focal narrowing of retinal
arterioles + AV nicking
3. Group 3: Group 2 + flame-shaped haemorrhages
+ cotton-wool spots + hard exudates
4. Group 4: Group 3 + optic disc swelling

36. Approach of case
 Age of patient
 Duration
 State of BP control
 Systemic disease
 Any treatment history

37. Examinations
 Vision
 IOP
 Dilated fundus examination
 Fundus photography
 FFA, OCT

38. Management
 The management of hypertensive retinopathy
depends on the severity of the disease:
 Mild hypertensive retinopathy:
The treatment consists of controlling of BP with
regular monitoring.

39.  Moderate Hypertensive Retinopathy:
1. Referral to a physician is essential to exclude
other associated factors like diabetes mellitus and
to check for any cardiovascular abnormalities.
2. Routine care including BP control and monitoring
is a must.

40.  Severe hypertensive retinopathy:
Requires urgent treatment and referral as it has
the strongest association with mortality.
Other systems such as renal, cardiovascular, and
brain should be monitored for signs of TOD.

41. General Treatment goals
 The treatment for moderate to severe
hypertensive retinopathy is to reduce the mean
arterial pressure by 10-15% in the first hour.
 Blood pressure should be lowered in a controlled
manner and by no more than 25% compared to
baseline by the end of the first day of treatment to
prevent further ischemic damage to target end
organs.

42.  Initial treatment often requires parenteral
antihypertensive agents and then transitioned to
oral agents.
 Goal-oriented hypertension treatment aims to
lower systolic blood pressure to < 130 mmHG and
diastolic pressure to < 80 mm Hg over the next 2-3
months.

43. Medical Therapy
 Drugs that are commonly used in the outpatient
setting to reduce blood pressure include angiotensin
converting enzyme inhibitors, calcium channel
blockers, and diuretics.
 Other less commonly used medications include α-
adrenergic blockers, direct vasodilators, and central
α2-adrenergic agonists.

44.  The patient should be followed by his primary
physician closely for management of hypertension.
 Intravitreal antibody treatment against vascular
endothelial growth factor (bevacizumab) for acute
hypertensive retinopathy to reduce macular edema
and retinal hemorrhage.

45. Complications of HTN retinopathy
 Retinal artery occlusion
 Retinal vein occlusion
 Anterior ischemic optic neuropathy
 Age-related macular degeneration
 Retinal arteriolar emboli
 Epiretinal membrane formation
 Cystoid macular edema

46. Conditions that mimic chronic
Hypertensive retinopathy are:
 Diabetic retinopathy
 Retinal venous obstruction
 Hyper viscosity syndrome
 Ocular ischemic syndrome
 Radiation retinopathy

47. Prognosis
 Chronic hypertensive retinopathy rarely causes
significant visual loss.
 The retinal changes can be halted when hypertension
is treated but arteriolar narrowing and AV changes
persist.
 For untreated malignant hypertension, the mortality
is high as 50% within 2 months of diagnosis and
almost 90% by the end of 1 year

48.  Vision loss in hypertensive retinopathy is because of
either
1. Secondary optic atrophy after prolonged
papilloedema
2. Retinal pigmentary changes after exudative retinal
detachment.

49. Pregnancy induced Hypertension
 Hypertension in pregnancy is a systolic blood
pressure ≥ 140 mmHg or diastolic blood pressure ≥
90 mmHg or both.
 Both systolic and diastolic blood pressure raises are
important in the identification of Pregnancy
induced hypertension

50.  Usually seen after 20 wks of Gestation
 Preeclampsia is associated with protenuria along
with HTN

51. Features of PIH retinopathy
 Reduced arteriolar caliber and arteriovenous ratio,
 Retinal hemorrhages and edema,
 Cotton wool spots secondary to arteriolar damage,
 Choroidal dysfunction with secondary RPE
damage,
 Serous retinal detachment,
 Vitreous hemorrhage.

52. Features of PIH retinopathy

53. Hypertensive choroidopathy
 Hypertensive choroidopathy is less common than
retinal hemorrhages and infarcts seen with
accelerated hypertension.
 The manifestations of choroidopathy include
serous retinal detachment, Elschnig spots, and
Siegrist streaks.

54.  Elschnig spots are yellow demarcated lesions in the
perimacular region that leak fluorescein after
occlusion of the choriocapillaris.
 When the Elschnig spot heals, a pigment spot is
left surrounded by a depigmented pale halo.
 Siegrist streaks are linear hyperpigmented streaks
over choroidal arteries.

55. Elsching’s spots

56.  Siegrist streaks tend to
appear as sclerosed
choroidal vessels with
overlying necrosis of
the choriocapillaris,
which leads to
secondary RPE atrophy

57.  Malignant hypertension can also cause choroidopathy.
Fibrinoid necrosis of choroidal arterioles leads to
segmental infarction of choriocapillaris.[10] Poor
perfusion of the choriocapillaris causes Elschnig spots,
defined as hyperpigmented patches in the choroid
surrounded by a ring of hypopigmentation, or Siegrist
streaks, defined as linear hyperpigmented lesions over
choroidal arteries. Hypertensive choroidopathy can
cause a focal pigment epithelium detachment, leading
to exudative retinal detachment.[4] Generally,
hypertensive choroidopathy affects younger patients
with malignant hypertension.[13]

58.  Uncontrolled high blood pressure is one of the
main causes of malignant hypertension. Other
causes include: Adrenal disorders including Conn's
syndrome, Cushing's syndrome,
pheochromocytoma or a renin-secreting tumor.

59. References
 Clinical ophthalmology by JJ kanski
 Eye Wiki By AAO
 Thank you