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Most patients with hypertensive retinopathy have no symptoms. However, some may report decreased or blurred vision, and headaches.
There is an association between the grade of retinopathy and mortality. In a classic study in 1939 Keith and colleagues described the prognosis of people with differing severity of retinopathy. They showed 70% of those with grade 1 retinopathy were alive after 3 years whereas only 6% of those with grade 4 survived.The most widely used modern classification system bears their name. The role of retinopathy grading in risk stratification is debated, but it has been proposed that individuals with signs of hypertensive retinopathy signs, especially retinal hemorrhages, microaneurysms and cotton-wool spots, should be assessed carefully.
Many people often do not have symptoms until very late in their disease course. Patients often become symptomatic when there is irreversible damage. Symptoms are usually not painful and can include:
- Vitreous hemorrhage
- Floaters, or small objects that drift through the field of vision
- Decreased visual acuity
- "Curtain falling" over eyes
Diabetic retinopathy often has no early warning signs. Even macular edema, which can cause rapid vision loss, may not have any warning signs for some time. In general, however, a person with macular edema is likely to have blurred vision, making it hard to do things like read or drive. In some cases, the vision will get better or worse during the day.
In the first stage which is called non-proliferative diabetic retinopathy (NPDR) there are no symptoms, the signs are not visible to the eye and patients will have 20/20 vision. The only way to detect NPDR is by fundus photography, in which microaneurysms (microscopic blood-filled bulges in the artery walls) can be seen. If there is reduced vision, fluorescein angiography can be done to see the back of the eye. Narrowing or blocked retinal blood vessels can be seen clearly and this is called retinal ischemia (lack of blood flow).
Macular edema in which blood vessels leak their contents into the macular region can occur at any stage of NPDR. The symptoms of macular edema are blurred vision and darkened or distorted images that are not the same in both eyes. Ten percent (10%) of diabetic patients will have vision loss related to macular edema. Optical Coherence Tomography can show the areas of
retinal thickening (due to fluid accumulation) of macular edema.
In the second stage, abnormal new blood vessels (neovascularisation) form at the back of the eye as part of "proliferative diabetic retinopathy" (PDR); these can burst and bleed (vitreous hemorrhage) and blur the vision, because these new blood vessels are fragile. The first time this bleeding occurs, it may not be very severe. In most cases, it will leave just a few specks of blood, or spots floating in a person's visual field, though the spots often go away after a few hours.
These spots are often followed within a few days or weeks by a much greater leakage of blood, which blurs the vision. In extreme cases, a person may only be able to tell light from dark in that eye. It may take the blood anywhere from a few days to months or even years to clear from the inside of the eye, and in some cases the blood will not clear. These types of large hemorrhages tend to happen more than once, often during sleep.
On funduscopic exam, a doctor will see cotton wool spots, flame hemorrhages (similar lesions are also caused by the alpha-toxin of "Clostridium novyi"), and dot-blot hemorrhages.
Retinopathy is any damage to the retina of the eyes, which may cause vision impairment. Retinopathy often refers to retinal vascular disease, or damage to the retina caused by abnormal blood flow. Age-related macular degeneration is technically included under the umbrella term retinopathy but is often discussed as a separate entity. Retinopathy, or retinal vascular disease, can be broadly categorized into proliferative and non-proliferative types. Frequently, retinopathy is an ocular manifestation of systemic disease as seen in diabetes or hypertension. Diabetes is the most common cause of retinopathy in the U.S. as of 2008. Diabetic retinopathy is the leading cause of blindness in working-aged people. It accounts for about 5% of blindness worldwide and is designated a priority eye disease by the World Health Organization.
Diabetic retinopathy, also known as diabetic eye disease, is a medical condition in which damage occurs to the retina due to diabetes and is a leading cause of blindness.
It affects up to 80 percent of people who have had diabetes for 20 years or more. At least 90% of new cases could be reduced if there were proper treatment and monitoring of the eyes. The longer a person has diabetes, the higher his or her chances of developing diabetic retinopathy. Each year in the United States, diabetic retinopathy accounts for 12% of all new cases of blindness. It is also the leading cause of blindness for people aged 20 to 64 years.
This condition is often associated with diabetes in advanced proliferative diabetic retinopathy. Other conditions causing rubeosis iridis include central retinal vein occlusion, ocular ischemic syndrome, and chronic retinal detachment.
The eyes may show retinal hemorrhage or an exudate. Papilledema must be present before a diagnosis of malignant hypertension can be made. The brain shows manifestations of increased intracranial pressure, such as headache, vomiting, and/or subarachnoid or cerebral hemorrhage. Patients will usually suffer from left ventricular dysfunction. The kidneys will be affected, resulting in hematuria, proteinuria, and acute renal failure. It differs from other complications of hypertension in that it is accompanied by papilledema. This can be associated with hypertensive retinopathy.
Other signs and symptoms can include:
- Chest pain
- Arrhythmias
- Headache
- Epistaxis
- Dyspnea
- Faintness or vertigo
- Severe anxiety
- Agitation
- Altered mental status
- Paresthesias
- Vomiting
Chest pain requires immediate lowering of blood pressure (such as with sodium nitroprusside infusions), while urgencies can be treated with oral agents, with the goal of lowering the mean arterial pressure (MAP) by 20% in 1–2 days with further reduction to "normal" levels in weeks or months. The former use of oral nifedipine, a calcium channel blocker, has been strongly discouraged as it has led to excessive falls in blood pressure with serious and fatal consequences.
Sometimes, the term hypertensive emergency is also used as a generic term, comprising both hypertensive "emergency", as a specific term for a serious and urgent condition of elevated blood pressure, and hypertensive urgency, as a specific term of a less serious and less urgent condition (the terminology hypertensive "crisis" is usually used in this sense).
Rubeosis iridis, also called neovascularization of the iris (NVI), is a medical condition of the iris of the eye in which new abnormal blood vessels (formed by neovascularization) are found on the surface of the iris.
The term hypertensive emergency is primarily used as a specific term for a hypertensive crisis with a diastolic blood pressure greater than or equal to 120 mmHg or systolic blood pressure greater than or equal to 180 mmHg. Hypertensive emergency differs from hypertensive crisis in that, in the former, there is evidence of acute organ damage.
Angiopathy is the generic term for a disease of the blood vessels (arteries, veins, and capillaries). The best known and most prevalent angiopathy is diabetic angiopathy, a common complication of chronic diabetes.
Hypertensive encephalopathy is most commonly encountered in young and middle-aged people who have hypertension. Overall, the condition is rare even among people with hypertension. Studies report that from 0.5 to 15% of people with malignant hypertension develop hypertensive encephalopathy. With the development of methods for detection and treatment of hypertension, hypertensive encephalopathy has been becoming more rare.
Symptoms of hypertensive encephalopathy typically start to occur 12–48 hours after a sudden and sustained increase in blood pressure. The first manifestation of these symptoms is a severe headache. Headache occurs in greater than 75% of patients. The patient becomes restless. Alterations in consciousness may follow several hours later, which include impaired judgement and memory, confusion, somnolence and stupor. If the condition is not treated, these neurological symptoms may worsen and ultimately turn into a coma. Other symptoms may include increased irritability, vomiting, diplopia, seizures, twitching and myoclonus of the limbs. Alterations in vision (vision blurring, hemivisual field defects, color blindness, cortical blindness) are common. They occur in 4 out of 11 cases (Jellinek et al. 1964). Hemiparesis, intracerebral hemorrhage, aphasia may also occur, but they are less common.
Prognosis is generally poor for all forms of Diabetic angiopathy, as symptomatology is tied to the advancement of the underlying pathology i.e. the early-stage patient displays either non-specific symptoms or none at all.
"Diabetic dermopathy" is a manifestation of diabetic angiopathy. It is often found on the shin.
There is also Neuropathy; also associated with diabetes mellitus; type 1 and 2.
Vitreous hemorrhage is the extravasation, or leakage, of blood into the areas in and around the vitreous humor of the eye. The vitreous humor is the clear gel that fills the space between the lens and the retina of the eye. A variety of conditions can result in blood leaking into the vitreous humor, which can cause impaired vision, floaters, and photopsia.
Patients with idiopathic macular telangiectasia type 1 are typically 40 years of age or older. They may have a coincident history of ischemic vascular diseases such as diabetes or hypertension, but these do not appear to be causative factors.
Macular telangiectasia type 2 usually present first between the ages of 50 and 60 years, with a mean age of 55–59 years. They may present with a wide range of visual impact, from totally asymptomatic to substantially impaired; in most cases however, patients retain functional acuity of 20/200 or better. Metamorphopsia may be a subjective complaint. Due to the development of paracentral scotomota (blind spots), reading ability is impaired early in the disease course. It might be even the first symptom of the disease.
The condition may remain stable for extended periods, sometimes interspersed with sudden decreases in vision. Patients’ loss of visual function is disproportionately worse than the impairment of their visual acuity, which is only mildly affected in many cases. In patients with MacTel, as compared with a reference population, there is a significantly higher prevalence of systemic conditions associated with vascular disease, including history of hypertension, history of diabetes, and history of coronary disease. MacTel does not cause total blindness, yet it commonly causes gradual loss of the central vision required for reading and driving.
Diabetic angiopathy is a form of angiopathy associated with diabetic complications. While not exclusive, the two most common forms are Diabetic retinopathy and Diabetic nephropathy, whose pathophysiologies are largely identical.
It is also possible to classify angiopathy by the associated condition:
- Diabetic angiopathy
- Congophilic angiopathy
The most common cause found in adults is diabetic retinopathy. Abnormal blood vessels can form in the back of the eye of a person with diabetes. These new blood vessels are weaker and prone to breaking and causing hemorrhage. Diabetic retinopathy accounts for 31.5-54% of all cases of vitreous hemorrhage in adults in the United States.
Hypertension with certain specific additional signs and symptoms may suggest secondary hypertension, i.e. hypertension due to an identifiable cause. For example, Cushing's syndrome frequently causes truncal obesity, glucose intolerance, moon face, a hump of fat behind the neck/shoulder (referred to as a buffalo hump), and purple abdominal stretch marks. Hyperthyroidism frequently causes weight loss with increased appetite, fast heart rate, bulging eyes, and tremor. Renal artery stenosis (RAS) may be associated with a localized abdominal bruit to the left or right of the midline (unilateral RAS), or in both locations (bilateral RAS). Coarctation of the aorta frequently causes a decreased blood pressure in the lower extremities relative to the arms, or delayed or absent femoral arterial pulses. Pheochromocytoma may cause abrupt ("paroxysmal") episodes of hypertension accompanied by headache, palpitations, pale appearance, and excessive sweating.
Hypertension is rarely accompanied by symptoms, and its identification is usually through screening, or when seeking healthcare for an unrelated problem. Some with high blood pressure report headaches (particularly at the back of the head and in the morning), as well as lightheadedness, vertigo, tinnitus (buzzing or hissing in the ears), altered vision or fainting episodes. These symptoms, however, might be related to associated anxiety rather than the high blood pressure itself.
On physical examination, hypertension may be associated with the presence of changes in the optic fundus seen by ophthalmoscopy. The severity of the changes typical of hypertensive retinopathy is graded from I–IV; grades I and II may be difficult to differentiate. The severity of the retinopathy correlates roughly with the duration or the severity of the hypertension.
Putscher's retinopathy is a disease where part of the eye (retina) is damaged. Usually associated with severe head injuries, it may also occur with other types of trauma, such as long bone fractures, or with several non-traumatic systemic diseases. However, the exact cause of the disease is not well understood. There are no treatments specific for Purtscher's retinopathy, and the prognosis varies. The disease can threaten vision, sometimes causing temporary or permanent blindness.
It is named for the Austrian ophthalmologist, Othmar Purtscher (1852–1927), who detected it in 1910 and described it fully in 1912.
Macular telangiectasia type 1 must be differentiated from secondary telangiectasis caused by retinal vascular diseases such as retinal venous occlusions, diabetic retinopathy, radiation retinopathy, sickle cell maculopathy, inflammatory retinopathy/Irvine–Gass syndrome, ocular ischemic syndrome/carotid artery obstruction, hypertensive retinopathy, polycythemia vera retinopathy, and localized retinal capillary hemangioma. In addition, Macular telangiectasia type 1 should be clearly differentiated from dilated perifoveal capillaries with evidence of vitreous cellular infiltration secondary to acquired inflammatory disease or tapetoretinal dystrophy. Less commonly, macular telangiectasis has been described in association with fascioscapulohumeral muscular dystrophy, incontinentia pigmenti, and familial exudative vitreoretinopathy with posterior pole involvement.
Macular telangiectasia type 2 is commonly under-diagnosed. The findings may appear very similar to diabetic retinopathy, and many cases ave been incorrectly ascribed to diabetic retinopathy or age-related macular degeneration. Recognition of this condition can save an affected patient from unnecessarily undergoing extensive medical testing and/or treatment. MacTel should be considered in cases of mild paramacular dot and blot hemorrhages and in cases of macular and paramacular RPE hyperplasia where no other cause can be identified.
Severely elevated blood pressure (equal to or greater than a systolic 180 or diastolic of 110—sometimes termed malignant or accelerated hypertension) is referred to as a "hypertensive crisis", as blood pressure at this level confers a high risk of complications. People with blood pressures in this range may have no symptoms, but are more likely to report headaches (22% of cases) and dizziness than the general population. Other symptoms accompanying a hypertensive crisis may include visual deterioration due to retinopathy, breathlessness due to heart failure, or a general feeling of malaise due to kidney failure. Most people with a hypertensive crisis are known to have elevated blood pressure, but additional triggers may have led to a sudden rise.
A "hypertensive emergency" is diagnosed when there is evidence of direct damage to one or more organs as a result of severely elevated blood pressure greater than 180 systolic or 120 diastolic. This may include hypertensive encephalopathy, caused by brain swelling and dysfunction, and characterized by headaches and an altered level of consciousness (confusion or drowsiness). Retinal papilledema and/or fundal bleeds and exudates are another sign of target organ damage. Chest pain may indicate heart muscle damage (which may progress to myocardial infarction) or sometimes aortic dissection, the tearing of the inner wall of the aorta. Breathlessness, cough, and the coughing up of blood-stained sputum are characteristic signs of pulmonary edema, the swelling of lung tissue due to left ventricular failure an inability of the left ventricle of the heart to adequately pump blood from the lungs into the arterial system. Rapid deterioration of kidney function (acute kidney injury) and microangiopathic hemolytic anemia (destruction of blood cells) may also occur. In these situations, rapid reduction of the blood pressure is mandated to stop ongoing organ damage. In contrast there is no evidence that blood pressure needs to be lowered rapidly in hypertensive urgencies where there is no evidence of target organ damage and over aggressive reduction of blood pressure is not without risks. Use of oral medications to lower the BP gradually over 24 to 48h is advocated in hypertensive urgencies.
A hypertensive urgency is a clinical situation in which blood pressure is very high (e.g., ≥180/≥110 mmHg) with minimal or no symptoms, and "no" signs or symptoms indicating acute organ damage. This contrasts with a hypertensive emergency where severe blood pressure is accompanied by evidence of progressive organ or system damage.
Where trauma is involved, only a funduscopic examination of the back of the eye (retina) is necessary to make the diagnosis. Fluoroscein angiography may show a decrease in blood flow to the areas of whiteness in the retina.