Hypertensive Retinopathy
Hypertensive retinopathy is a form of target-organ damage caused by systemic hypertension. It is characterised by retinal vascular damage secondary to sustained or abrupt elevations in systemic blood pressure, producing visible changes on fundoscopy.
This updated UKMLA guide to hypertensive retinopathy covers causes, risk factors, symptoms, diagnosis, staging, and management.
Pathophysiology
Hypertensive retinopathy is primarily driven by arteriosclerosis (thickening and stiffening of arterioles) alongside the mechanical stress of hypertension.
Causes and Risk Factors
The primary cause is sustained or abrupt elevations in systemic blood pressure, which can result from:
- Primary (essential) hypertension, or
- Secondary hypertension (e.g. CKD, endocrine disorders – see the Secondary Hypertension article for more information)
Key risk factors:
- Duration and severity of hypertension – most significant predictors
- Males
- Older age
- Concurrent medical conditions (e.g. diabetes, CKD, dyslipidaemia)
- Smoking
- Obesity
- Afro-Caribbean, African American, or Chinese descent
Clinical Features
Often asymptomatic
Symptoms often only arise if hypertension is severe:
- Bilateral visual decline or dimness of vision
- Headaches
Complications
Hypertensive retinopathy increases the risk of:
- Vascular occlusions (CRVO and CRAO)
- Retinal detachment (often bilateral, occurring in young patients with poorly controlled, malignant hypertension)
- Optic atrophy and vision loss (from prolonged papilloedema)
Investigation and Diagnosis
Hypertensive retinopathy is often detected during routine target organ damage assessment in hypertension via fundoscopy.
Key retinal changes and classification (Keith-Wagener-Barker System):
| Grade 1 | Slight generalised narrowing or sclerosis of retinal arterioles |
| Grade 2 | Arteriovenous (AV) nicking
Distinct arteriole narrowing |
| Grade 3 | Grade 2 features PLUS
|
| Grade 4 | Grade 3 features PLUS papilloedema |
Arteriolar narrowing can result in changes in the vessel wall reflex:
- Copper wiring: increased light reflex gives the vessel a burnished look
- Silver wiring: seen in advanced stages where the vessel wall becomes completely opaque, obscuring the blood column inside and resembling a white cord
Retinal haemorrhages:
- Flame-shaped haemorrhages are more superficial, in the nerve fibre layer
- Dot-blot haemorrhages are deeper in the retina
Exudates:
- Soft exudates (cotton-wool spots) represent areas of micro-infarction from ischaemic nerve fibre damage (not true exudates)
- Hard exudates are bright, yellow lipid deposits that leak into the retina (due to breakdown of blood-retinal barrier and vessel leakage)
Some key fundoscopic findings that differentiate between hypertensive and diabetic retinopathy:
| Feature | Hypertensive retinopathy | Diabetic retinopathy |
|---|---|---|
| Papilloedema | Yes (grade 4) | No |
| AV nicking | Yes (grade 2) | No |
| Microaneurysms | No | Yes |
| Neovascularisation | No | Yes |
Management
Note: Severe hypertension (BP ≥180/120 mmHg) with retinal haemorrhages and/or papilloedema is referred to as accelerated/malignant hypertension.
This is managed as a hypertensive crisis and is covered in the Hypertensive Crisis article.
Hypertensive retinopathy doesn’t usually require active intra-ocular treatment, apart from:
- Optimise blood pressure control – see the Hypertension (Primary) article
- Regular monitoring
Most cases of severe changes like papilloedema respond well to blood pressure control alone.
If severe subfoveal fluid persists, intravitreal anti-VEGF therapy (like bevacizumab) may be considered in secondary care.