Hypertensive retinopathy, formerly termed as "albuminuric retinitis", is a condition characterized by appearance of a series of changes in the retinal vasculature occurring as a result of acutely severe or prolonged, consistent systemic hypertension.
The signs and symptoms of hypertensive retinopathy usually develop in later stages of the disease. Most patients are asymptomatic although some may present with headaches, blurred vision or loss of vision. In emergency situations, symptoms of stroke may start to appear which requires immediate hospitalisation and prompt management.
The fundoscopic examination of patients in earlier stages of the disease reveals constriction of arterioles. Findings that present with chronic, prolonged hypertension include arteriovenous nicking and vascular wall changes that are identified by copper wiring and silver wiring.
In acute, severe cases of hypertensive retinopathy characteristic flame-shaped hemorrhages, cotton wool spots, yellow hard exudates and optic disk edema are identified during examination. Generalized signs of extravascular lesions that accompany hypertensive retinopathy include microaneurysms, retinal hemorrhages, edema of retina and macula, lipid deposition on retina and focal intraretinal periarteriolar transudates (FIPTs).
Diagnosis of hypertensive retinopathy is based on patient's history, retinal examination and fundoscopy. Routine opthalamoscopic examination is recommended in patients with stage III hypertension, in hypertensive patients presenting with visual symptoms and in general case of sustained hypertension. Alternatively, retinal changes can also be assessed through advanced digital photography of retinal structure using specialized software. Other diagnostic tools that have been used are the Keith and Scheie staging scales, although they do not indicate considerable changes in retinal structures of hypertensive patients.
Hypertension is the primary cause for the development of hypertensive retinopathy. Therefore, controlling hypertension is the first step in the management of the disease. It is imperative to keep blood pressure within normal range by keeping regular checks, getting periodic evaluation by a physician, dietary and lifestyle modifications and pharmacotherapy with prescribed antihypertensives. Mild damage to the retina resulting from acute hypertensive episode can be reversed. Complications like loss of vision require treatment with laser or administration of corticosteroids and antivascular endothelial growth factor drugs by the intravitreal route. Monoclonal antibodies ranibizumab and bevacizumab and pegaptanib are the recommended antivascular endothelial growth factors.
All hypertensive patients who are at risk of developing optic neuropathy or are already suffering from optic neuropathy must avoid sudden decline in blood pressure. The persistently elevated blood pressure in the vessels supplying optic nerve are autoregulated by adjusting blood supply according to higher blood pressure. Therefore, sudden decline in blood pressure cuts off the blood supply to the optic nerve causing nerve tissues to die.
Timely diagnosis of hypertensive retinopathy is the key to limit worsening of retinal damage and avoid structural changes to optic nerve and macula. Once the retinal blood vessels undergo arteriosclerosis, further risks for developing retinal artery and vein occlusions and retinal microaneurysms become inevitable which in turn may precipitate peripheral vascular disease, coronary artery disease and stroke in the long run. Therefore, earlier diagnosis and management provides positive outcome with good prognosis.
Elevated blood pressure has been considered the leading cause in the development of retinal hypertension. Combined with diabetes mellitus, hypertension greatly raises the risk of vision loss. The risk of damage to other organs is increased in patients with hypertensive retinopathy. Smoking, although not a risk factor for hypertensive retinopathy, is thought to worsen the condition.
In a report published by the Beaver Dam Eye Study, it has been indicated that chronic hypertension is responsible for causing vascular changes in the retina, resulting in narrowing of arterioles and venules . In a Beijing Eye Study, it was observed that generalized arteriolar narrowing and focal arteriolar narrowing occurs in 25.4% and 12.1% of patients with hypertension respectively . Incidence of increased blood pressure in childhood can precipitate hypertension in young people during adulthood, leading to retinal hypertension.
Epidemiological studies have indicated that 3%-14% of non-diabetic individuals above 40 years of age suffer from hypertensive retinopathy, 12% of which develop focal narrowing of arterioles while 3%-17% have retinal hemorrhages  although non-hypertensive patients may also present with pathological modifications in retinal vasculature after 40 years.
A spectrum of focal and generalized signs occur in hypertensive retinopathy owing to autoregulatory physiological response by retinal vasculature due to elevated blood pressure (in acute phases). As hypertensive retinopathy progresses, the autoregulation mechanism becomes disrupted as the consistent rise in blood pressure causes structural and functional changes in the retinal arterioles (in chronic cases)  .
In acute phases, temporary vasoconstriction occurs in the terminal retinal vasculature which causes narrowing of retinal arterioles as a result of physiological autoregulation. In chronic systemic hypertension, damage to vascular endothelium and cell necrosis cause visible and irreversible arteriosclerotic changes in the retinal vasculature. In severely prolonged hypertension that persists for years, other vascular changes further ensue which include localized signs of hypertensive retinopathy such as arteriolar wall thickening, arteriovenous nicking, microaneurysms, retinal hemorrhage and cotton wool spots and diffuse signs that comprise generalized arteriolar narrowing and arteriolar wall opacification .
Focal narrowing of retinal arterioles occurs due to vasospasm or edema of the retinal arterioles resulting from increase in intraluminal pressure whether in the retinal arterioles or in the central artery of the retina. Development of arteriosclerotic changes in chronic hypertension cause further sclerosis and hyalinization of retinal arterioles which causes them to become red-brown, a phenomenon known as copper wiring. When the hypertension continues for years, sheathing of vessels occurs by progression of arteriolar sclerosis to a more advanced stage. Sheathing of vessel wall is characterized by increase in optical density which further leads to pipe-stem sheathing in which the entire surface of vessel becomes opaque followed by vascular wall involvement, which ultimately produces a silver-wire vessel. Arteriovenous nicking occurring in prolonged hypertenion results from hindrance in blood circulation causing dilatation of retinal vein and hourglass constrictions, a phenomenon known as the Gunn sign. Cotton wool spots are small clogs present on the inner layer of retinal vessels where they appear as fluffy, white lesions. The spots are indication of small localized ischemic stroke of retinal blood vessels due to elevated blood pressure. Cotton wool spots typically appear in later stages of retinal hypertension with prolonged hypertension and last for about 3-6 weeks but reappear if hypertension persists, causing further damage .
Controlling blood pressure is they key to prevent occurrence of hypertensive retinopathy later in life. Adopting a healthy lifestyle that includes incorporating healthy diet devoid of excess sugar and cholesterol, regular exercise, maintenance of healthy weight and getting regular examination from a physician help prevent end organ damage, including retinopathy. Following prescribed regimen of antihypertensive therapy is paramount in keeping sudden hypertensive episodes at bay.
Hypertensive retinopathy, a state of target organ damage as indicated by the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII)  is referred to as damage to retinal vasculature as a result of systemic arterial hypertension. The series of ensuing retinal vascular changes develop on prolonged, severe and sustained hypertension  and are characterized by vascular exudations, arteriosclerosis (causing vascular narrowing), vascular leakage and retinal edema.
Several international guidelines have categorized hypertensive retinopathy by providing grading systems. The European Society of Hypertension-European Society of Cardiology Guidelines (ESH-ESC 2003), the WHO International Society of Hypertension (WHO-ISH) 2003 and the British Hypertension Society 2004 Guidelines (BHS IV) have regarded that hypertensive retinopathy produces clinical signs in grades III and IV   .
Hypertensive retinopathy produce focal and generalized signs on progression. Initially, arteriolar narrowing occurs followed by arteriosclerosis and disruption of the blood-retinal barrier in sustained, untreated hypertension. Increased vascular permeability and leakage follows which ultimately results in small retinal hemorrhages, hard exudates and retinal edema. Papilledema is another finding that is specific to accelerated hypertension.
Treatment and preventing progression of the disease is directed at controlling blood pressure. Hypertensive retinopathy is a preventable illness since end organ damage can be prevented by treating hypertension from the very start with antihypertensives and basic lifestyle modifications.
Hypertensive retinopathy is a condition secondary to high blood pressure in which the retina of the eye, a light sensitive transparent structure present behind the eye ball, is damaged. The blood vessels that supply blood to the retina are damaged during high blood pressure which causes hindrance in the flow of blood through those vessels and reduces blood supply to a large extent. With insufficient supply of blood, some areas of the retina become damaged and small patches or spots appear on the retina, indicating minor hemorrhages. If left uncontrolled, blood may end up leaking into the retina in later course of the disease and cause loss of vision over the years.
In patients with diabetes, the risk for vision loss in hypertensive retinopathy increases by two fold. The condition is worsened by tobacco smoking. The disease has been found to occur in individuals above 40 years of age.
Correct diagnosis at the right time is of utmost importance in order to achieve good outcome. Early diagnosis can help in staying away from complications by initial management.
Hypertensive retinopathy is usually diagnosed by taking patient's history, retinal examination and fundoscopy. Hypertensive patients are advised to undergo routine opthalamoscopic examination even if minor signs of visual impairment appear. The opthalamoscope helps in observing physical appearance of the retina and detect minor changes in the eye structure during high blood pressure.
Treatment of hypertensive retinopathy is aimed at controlling blood pressure and keeping it on a lower side. Corticosteroid injections (Dexamethosone) and biological drugs (Ranibizumab, pegaptanib, aflibercept, bevacizumab) are commonly used medications.
Hypertensive retinopathy is completely preventable if the patients keep their blood pressure within control from the beginning. Taking regular medications, adopting a healthy life style with exercise and healthy diet and regular checks ups can easily prevent the development of hypertensive retinopathy.