Hypertensive Retinopathy

Dr Khoirom Yaifabi Chanu

Hypertensive Retinopathy

 A spectrum of clinical signs resulted by a range of pathophysiologic changes in

response to elevated blood pressure
 Hypertension has profound effect on both the structure and function of the
vasculature in the eye
Pathophysiology

 The ocular effects of hypertension arise from the impact on the ocular
vasculature
 Hypertension accelerates both arteriosclerosis and atherosclerosis
 No central regulation of blood flow occurs in the retina
 The retinal arteries and the arterioles remain in inner retina. Only capillaries are
found as deep as inner nuclear layer (same for retinal veins)
 When two vessels cross, artery usually lie anterior to the vein and the two
vessels share a common adventitial sheath.
 Crossings represent the most common site of branch retinal vein obstructions
 Retinal circulation depend upon local chemical autoregulation to maintain a
constant metabolic environment.
 Blood flow is controlled by the need for oxygen and the accumulation of
metabolic by-products such as CO2 and changes in PH
 (Choroid – blood flow is regulated by ANS)
 Optic nerve head vessels exhibit autoregulation but an incomplete blood ocular
barrier as a result of peripapillary choroidal vessels

 Because of the vascular differences between the retina, the choroid and the
optic nerve, each of these regions respond differently to hypertension.
Clinically divided into two types:
o Chronic hypertensive retinopathy:
 Asymptomatic
 Retinal vascular changes occurring from chronically elevated systemic arterial
blood pressure
 Signs include
 Arteriosclerosis leading to localised and generalised narrowing and irregularly
of vessels (tortuosity)
 Arteriovenous nicking
 Increased arteriolar light reflex
 Arteriolar light opacification
 Signs of venous stains such as retinal haemorrhages, macular edema and
cotton wool spots
 Venous occlusive disease and macroaneurysm
 Remodelling changes due to capillary non perfusion, such as shunt vessels and
microaneurysms
 Gunn sign: arteriovenous crossing, the arteriole presses upon the vein causing
hourglass constrictions on both sides
 Salu’s sign: due to increase in resistance to blood flow, the vein that crosses at an
acute angle normally, now cross by making a more obtuse angle.
 Flame shaped haemorrhages: posterior pole in retinal NFL; disappear in about 3-5
weeks
 Hard exudates: refractile yellow flat lesions; accumulation of plasma lipids; outer
plexiform layer
 Characteristic pattern like macular star and macular fan may also be seen;
temporary, disappear in 3-6 weeks
 Cotton wool spots or soft exudates
o Occlusion of terminal arterioles  Ischemic edema  Infarction of the
retinal nerve fibre layer
o More common at posterior pole
o Last 3-6 weeks fading away leaving retinal nerve fibre layer defects
o Hyperfluorescent in fluorescin angiography
 Differential diagnosis of chronic hypertensive retinopathy
 Diabetic retinopathy
 Retinal venous obstruction
 Hyperviscosity syndromes
 Congenital hereditary retinal artery tortuosity
 Ocular ischaemic syndrome
 Radiation retinopathy
Acute hypertensive retinopathy/Malignant
hypertensive retinopathy
 Symptoms  Signs
o Headache o Retinal arteriolar spasm
o Scotoma o Superficial retinal haemorrhage
o Diplopia o Cotton wool spots, FIPTS
o Decreased vision o Elchnig’s spots
o Photopsias o Serous retinal detachment
o Optic disc edema
Clinical findings are divided into three distinct categories
o Acute hypertensive retinopathy
 Marked arteriolar narrowing due to spasm of retinal arterioles
 Flame shaped haemorrhages are more in number as well as greater in severity
 Focal intraretinal periarteriolar transudates (FIPTS)
 Ensuing from focal dilatation of terminal retinal arterioles
 Small, white, focal, oval lesions
 Deep in the retina located along major arteriolar vessels
 Hyperfluorescent
 Cotton wool spots are characteristic and are larger in size and greater in number
 Microaneurysm, shunt vessels and collaterals due to capillary obliterations
Differential diagnosis of acute hypertensiveretinopathy

 Bilateral bullous central serous chorioretinopathy

 Bilateral central retinal vein obstruction
 Collagen vascular diseases
 Diabetic retinopathy
Acute hypertensive choroidopathy
 Causes infarction and damage to RPE cells due to vasoconstriction of choroidal
vessels
 Transudation of fluid into the subretinal space due to increased pressure in the
choroidal vessels
Acute hypertensive optic neuropathy
 Optic disc edema
 Haemorrhage on disc and peripapillary retina
 Vasoconstriction of the posterior ciliary artery supplying the optic nerve head leads
to ischaemia of the optic nerve leading to edema AION (anterior ischaemic optic
neuropathy)
Staging of hypertensive retinopathy
o Keith-Wagener-Barker classification
 Patients were grouped according to ophthalmoscopic findings
 Stage 1: slight narrowing
 Sclerosis
 Tortuosity of the retinal arterioles
 Stage 2: definite narrowing
 Focal constriction
 Sclerosis
 AV nicking
 Stage 3: 2+ cotton wool spots, hard exudates, haemorrhages
 Stage 4: 2+3+ Papilloedema
Treatment and prognosis
 Treatment of underlying systemic condition can halt the progress of retinal changes
however arteriolar narrowing and AV nicking are permanent
 Blood pressure should be lowered in a slow, deliberate and controlled fashion to
prevent end-organ damage
 (very rapid decline can lead to ischaemia of optic nerve, brain and other vital
organs)