This document discusses hypertensive retinopathy, including its clinical presentation, pathogenesis, staging, and fundus changes. It describes how long-standing hypertension can damage the retina, choroid, and optic nerve through vasoconstriction and increased vascular permeability. The staging systems of Keith Wagner and Wong-Mclntosh are outlined. Features of acute hypertensive retinopathy include cotton wool spots, flame-shaped hemorrhages, and exudates. Chronic changes include arteriolar narrowing, nicking, and sclerosis. Malignant hypertension can cause necrotizing retinitis and serous retinal detachment. Pregnancy-induced hypertension also causes a reversible retinopathy.
7. Chronic Hypertensive Retinopathy
1. HYPERTENSION WITH INVOLUTIONARY
(SENILE)SCLEROSIS
Augmented Arteriosclerotic Retinopathy >50 year Age
2..CHRONIC HYPERTENSION WITH COMPENSATORY
ARTERIOLAR SCLEROSIS
Young , prolioferative and fibrous change in the Tunica Media .
Compensatory arteriosclerotic sclerosis)
Albuminuric or Renal Retinopathy
17. flame-shaped hemorrhages in the superficial layers of the retina and cotton-
wool patches caused by occlusion of the precapillary arterioles with
ischemic infarction of the inner retina.
Long-standing hypertension can produce arteriolar sclerotic vascular
changes, such as copper or silver wiring of the arterioles, as shown by the
two arrows in the figure, or arteriorvenous nicking.
chronic hypertension is lipid exudates resulting from abnormal
vascular permeability, as shown by the arrow at left.
swelling of the optic disc, seen here by the blurring of the temporal disc
margins. Hallmark of malignant hypertension
.
18.
19. MALIGNANT HYPERTENSION
High BP Retinal vasculature lose auto regulation (190/120 mmHg))
Headache,Blurred vision , Altered sens,Dysnoea
• Acute Hypertensive Retinopathy –
Spasm of arteriole
Hyperplastic arteriosclerosis, concentric hyperplastic arteriosclerosis-
onion peeling – necrosis & inflammation- Necrotizing vsculitis
• Superficial Retinal Haemorhages
• Focal intraretinal periarteriolar transudates (FIPTS)-Due to
deposition of macro molecule along arteriole due blood
retinal barrier break ,Small white focal lesion
• Cotton wool spot
• Capillary Obliteration-Micro aneurysm,shunt vessels,
collateral
20.
21. Acute Hypertensive Choroidopathy –
• Acute ischemic change in choriocapillaries ,Focal white
spot
• Elschnig’s spot – Small black spot surrounded by yellow
haloes-Due to RPE infarction
• Siegrist streaks- fibrinoid necrosis pigment along
choroidal arteriole
• Serous Neurosensory Retinal Detachment
25. Acutely, the patient complains of mild bilateral visual loss and
blood pressure is 224/68 mmHg. Note the attenuation of retinal
arteries, dilation of the veins, cotton wool spots (soft exudates)
(white circle), flame shaped hemorrhages (white arrowheads), hard
exudates (white arrow), and Elschnig spots (star). There is macular
edema bilaterally, which explains the decreased visual acuity.
• Second row of photographs: Retinal fluorescein angiography
showing hyperfluorescence at the level of the Elschnig spots (star),
and microaneurysms (white arrows).
• Third row of photographs: Retinal appearance two weeks later
(after normalization of blood pressure). Note the improvement of
macular edema and the increased hard exudates.
• Bottom row of photographs: Three months later, the cotton wool
spots and retinal hemorrhages have resolved. The arterial
attenuation persists, and the veins are less dilated. Both optic
nerves have become slightly pale.
26.
27. Stage III/IV hypertensive retinopathy There is mild bilateral optic
nerve edema. Note the arteriovenous nicking (white arrows), the
flame hemorrhage (white arrowhead), the boat-shaped hemorrhage
(star), and the arteriolar narrowing (black arrows).
28. Severe stage IV hypertensive retinopathy with bilateral optic nerve head oedema in
the setting of malignant hypertension c.
29. Hypertensive choroidopathy
• Not possess the autoregulatory capacity of the retinal vasculature .
• Divided into three constrict, leading to necrosis of the
choriocapillaris and retinal pigment epithelium and the
accumulation of exudates in phases. During the acute ischemic
phase, choroidal arterioles he subretinal space. The clinical fundus
findings during this phase include white areas (a manifestation of
retinal pigment epithelium necrosis), and focal serous retinal
detachment most often involving the macula and peripapillary
region. Retinal fluorescein angiography shows patches of
hypoperfused choriocapillaris, particularly in the central region of
the macula.