Hypertension or raised blood pressure is usually considered when the reading exceeds 140mm of Hg (systolic) and 90mm of Hg (diastolic). It is recorded as 140/90mm of Hg. Treatment at this level depends upon risk of coronary events, presence of diabetes or end organ damage. All patients with malignant hypertension or a sustained blood pressure more than 160/100mm of Hg should be treated. Malignant hypertension refers to severe hypertension ( more than 200mm of Hg as systolic and more than 130mm of Hg as diastolic) in conjunction with bilateral retinal haemorrhages and exudates with or without papilloedema.
In hypertensive retinopathy, retinal arterioles (small diameter blood vessels joining arteries to capillaries) respond to systemic hypertension by narrowing. Narrowing depends upon the degree of pre-existent involutional sclerosis (fibrosis). Therefore, hypertensive narrowing in its pure form is seen in young individuals whereas less narrowing is seen in older individuals due to rigidity of vessels (caused by involutional sclerosis). In sustained systemic hypertension, there is vascular leakage due to disruption of blood-retinal barrier. Hypertensive retinopathy shows features of narrowing (Vasoconstriction), involutional sclerosis (arteriosclerosis) and leakage (haemorrhage, oedema and hard exudates).
Most of the patients do not show any symptoms.
Patients with malignant hypertension may present with headache, pain in the eye or reduced vision.
Involutional sclerosis as such does not produce any symptoms. However, complications of sclerosis like macro-aneurysms or vascular occlusions may produce symptoms.
Chronic hypertension leads to arteriosclerotic changes in the blood vessels.
Hypertension may be primary or essential for which there is no detectable cause.
Secondary hypertension may be caused by an underlying disease such as:
– Primary hyperaldosteronism.
– Cushing’s syndrome.
– Renal vascular or renal parenchymal disease.
– Coarctation of aorta.
Major risk factor for essential hypertension is the severity of hypertension. General risk factors are use of tobacco, alcohol, high salt diet, obesity and stress.
For arteriosclerotic hypertension, it is the duration of disease which is an important risk factor.
Diagnosis of hypertensive retinopathy is based on presence of systemic hypertension and examination of retina (by an eye specialist) after dilating the pupil.
Retinal or Fundus examination:
It may show:
– Narrowing of blood vessels (vasoconstriction): Blood vessels may show generalised or localised narrowing. Severe hypertension may lead to obstruction of arterioles and formation of cotton-wool spots.
– Leakage: Abnormal vascular permeability leads to retinal oedema, flame-shaped haemorrhages and formation of hard exudates. Hard exudates may be arranged as macular star around the fovea. There may be swelling of the optic nerve head as disc oedema in malignant hypertension.
– Arteriosclerosis: There is thickening of blood vessel wall. Thickening causes marked changes at arteriovenous crossings.
Hypertensive retinopathy is graded as (Keith-Wagener classification):
– Grade 1: It is characterised by mild generalised arteriolar narrowing and tortuosity, particularly of smaller branches, with broadening of arteriolar light reflex and concealment of vein.
– Grade 2: There is more severe generalised as well as focal arteriolar narrowing. There is deflection of veins at arteriovenous crossings (Salus’ sign).
– Grade 3: It consists of copper-wiring of arterioles, banking of veins distal to arteriovenous crossings (Bonnet’s sign), tapering of veins on both sides of arteriovenous crossings (Gunn’s sign) and right angled deviation of veins. Cotton wool spots, hard exudates and flame-shaped haemorrhages may also be present.
– Grade 4: Along with changes of grade 3, there may be silver-wiring of arterioles (due to further sclerosis) and disc swelling.
Systemic hypertension may show other ocular manifestations such as:
– Retinal artery occlusion.
– Branch retinal vein occlusion.
– Retinal arterial macroaneurysm.
– Ischaemic choroidal infarcts (Elschnig’s spots).
– Ischaemic optic neuropathy.
Fluorescein angiography test: Acute malignant hypertension on fluorescein angiography shows non-perfusion of retinal capillaries, microaneurysms and dendritic pattern of choroidal filling in early phase. There is diffuse leakage in late phase.
Systemic hypertension should be controlled as a primary measure for Hypertensive retinopathy.
Change in lifestyle with reduction of general risk factors (salt restriction, avoidance of tobacco) help in controlling hypertension.
Drugs may be used from groups like:
– Beta blockers.
– Angiotensin converting enzyme inhibitors.
– Calcium channel blockers.
– Angiotensin receptor antagonists.
Patients with severe hypertensive retinopathy are at increased risk of coronary artery disease, stroke or peripheral vascular disease. Arteriosclerotic changes increases the risk of retinal macroaneurysms, retinal artery or vein occlusion. Visual acuity may be reduced due to involvement of optic nerve and macula.
Hypertensive retinopathy with vision threatening complication: Vision threatening complications like retinal oedema may be treated with laser therapy or intravitreal injection of vascular endothelial growth factor (VEGF) drugs.
Management by drugs, lasers and intravitreal injection should be under supervision of a qualified doctor.