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Monday, May 10, 2010

Hypertensive retinopathy

Keith-Wagener-Barker Hypertensive Retinopathy Classifications

Stage 1: Mild retinal vascular changes (generalized arteriolar narrowing).
Stage 2: Moderate to severe retinal vascular changes (arteriovenous crossing changes).
Stage 3: Stage 1 and 2 findings, plus cotton-wool spots, retinal hemorrhages and exudates.Stage 4: Stage 3 findings, plus associated optic nerve head swelling and macular star formation.

Hypertensive choroidopathy manifests less often than HTR. Unlike the retinal vasculature system, the choriocapillaris are not autoregulated. They are thin with a high degree of fenestration, which makes them susceptible to severe acute rise in blood pressure.

Hypertensive choroidopathy is a sign of choroidal vascular insufficiency, resulting in choroidal and overlying retinal pigment epithelium (RPE) infarction. Focal ischemia within the choroidal vasculature results in occlusion of the choriocapillaris and leads to damage of the overlying RPE.

Two common manifestations of hypertensive choroidopathy are Elschnigs spot and Siegrists streak. Elschnigs spots are typically yellow circular lesions with associated hyperpigmentation, while Siegrists streaks are linear pigmented areas that run along sclerotic choroidal vessels.

Also, serous retinal detachment may occur in conjunction with hypertensive choroidopathy. Disruption of the RPE leads to a breakdown of the retinal blood barrier, which results in subretinal fluid accumulation.



RETINAL ARTERY MACROANEURYSM

Fifty percent to 75% of presenting retinal arterial macroaneurysms (RAM) are associated with HTN. Specifically, HTN contributes to vessel wall weakening and leads to aneurysm formation.19,20

A RAM is an acquired localized round dilation that balloons over a major retinal arterial branch (figure 5).
Typically, it has a unilateral presentation and affects women between the ages of 50 and 80 who have a systemic history of hypertension. Associated leakage in the form of exudation, retinal edema and hemorrhage may also be observed.

There are two distinct forms of RAMs. A fusiform RAM is spindle shaped, while a saccular RAM is shaped like a small sac.21 The saccular form is more likely to result in hemorrhaging, while the fusiform type is typically associated with exudation.

Also, the presentation of either form of RAM is unpredictable. It may present as a benign aneurysm, or it may be associated with variable layers of retinal hemorrhage, including vitreous hemorrhage.

Furthermore, weakening of the macroaneurysm wall may result in associated retinal edema and exudation in a circinate pattern. Although many patients initially are asymptomatic, macular involvement often leads to visual impairment.



Angiography aids in the diagnosis, showing hyperfluorescence filling of the RAM, with possible associated leakage and microvascular anomalies.

Because the bleeding typically results in spontaneous aneurysmal thrombosis and vessel sclerosis, asymptomatic or non-leaking RAMs should be monitored closelyevery six months.22
Non-leaking RAMs near the macula, or leaking RAMs that do not threaten the macula require even closer monitoring.

Treatment is considered for a leaking RAM near the macula and persistent or progressive RAMs, particularly if a pulsating arterial wall is noted. A pulsating RAM indicates a thin wall, which is more likely to rupture.

Treatment options include photocoagulation laser treatment and Nd:YAG photodisruption.23-25 Photocoagulation laser treatment seals the leaking aneurysm. On the other hand, Nd:YAG photodisruption assists absorption of the associated hemorrhage by creating a slit on the retinal surface that allows the hemorrhage to drain into the vitreous cavity. This process speeds up the recovery of vision and prevents irreversible damage associated with complications and longstanding toxicity of hemorrhage to the retina. Currently, all RAM treatments are controversial with variable results.23-25

Ocular Manifestations of Hypertension
Anterior ischemic optic neuropathy
Central or branch retinal artery occlusion (CRAO or BRAO)
Central or branch retinal vein
occlusions (CRVO or BRVO)
Choroidal infarction
Cranial nerve palsies
Progression of diabetic retinopathy
Glaucoma
Hypertensive retinopathy
Idiopathic polypoidal choroidal
vasculopathy (IPCV)
Macroaneurysms
Ocular ischemic syndrome
Subconjunctival hemorrhage
Transient visual obscurations
REFERENCES:

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