Edema is an abnormal accumulation of fluid in the interstitium, located beneath the skin and in the cavities of the body which cause severe pain. Clinically, edema manifests as swelling; the amount of interstitial fluid is determined by the balance of fluid homeostasis, and the increased secretion of fluid into the interstitium, or the impaired removal of the fluid can cause edema. Peripheral edema is edema (accumulation of fluid causing swelling) in tissues perfused by the peripheral vascular system, usually in the lower limbs. In the most dependent parts of the body (those hanging distally), it may be called dependent edema. The condition is commonly associated with aging, but can be caused by many other conditions, including congestive heart failure, trauma, alcoholism, altitude sickness, pregnancy, hypertension, sickle cell anemia, or merely long periods of time sitting or standing without moving. Some medicines (e.g. amlodipine, pregabalin) may also cause or worsen the condition. Cerebral edema or cerebral oedema is excess accumulation of fluid in the intracellular or extracellular spaces of the brain. Certain changes in morphology are associated with cerebral edema: the brain becomes soft and smooth and overfills the cranial vault, gyri (ridges) become flattened, sulci (grooves) become narrowed, and ventricular cavities become compressed. Symptoms include nausea, vomiting, blurred vision, faintness, and in severe cases, seizures and coma. If brain herniation occurs, respiratory symptoms or respiratory arrest can also occur due to compression of the respiratory centers in the pons and medulla oblongata.
No outcomes found in Brazil. The prevalence of DME among US diabetics approaches 30% in adults who have had diabetes for 20 years or more and varies with the stage of diabetic retinopathy. It can occur at any stage of diabetes and can predate the appearance of other findings of diabetic retinopathy. In eyes with mild nonproliferative retinopathy, the prevalence of DME is 3%. This rises to 38% in eyes with moderate to severe nonproliferative retinopathy, and reaches 71% in eyes with proliferative retinopathy. Untreated, 20% to 30% of patients with DME will experience a doubling of the visual angle within 3 years; with current treatment, this risk drops by 50%. Diabetic retinopathy becomes nearly ubiquitous with long-standing diabetes. After 20 years with the disease, 60% of type 2 diabetics and virtually 100% of type 1 diabetics will manifest some form of retinopathy. Poor control of blood sugar increases the risk of diabetic retinopathy, and diabetic nephropathy may be a marker for retinopathy. Systemic hypertension is a risk factor for the development of both diabetic retinopathy and DME, and hyperlipidemia increases the risk of leakage and exudative deposits in the macula.
Treatment approaches can include osmotherapy using mannitol, diuretics to decrease fluid volume, corticosteroids to suppress the immune system, and surgical decompression to allow the brain tissue room to swell without compressive injury. Treatment involves resolving the underlying cause. Treatment may also involve positioning the affected body parts to improve drainage. For example, swelling in feet or ankles may be reduced by having the person lie down in bed or sit with the feet propped up on cushions. Intermittent pneumatic compression can be used to pressurize tissue in a limb, forcing fluids to flow out of pressurized area. Anti-VEGF drugs are effective compared to both laser and placebo and seem to be more effective than steroids in improving BCVA. They have been shown to be safe in the short term but require frequent injections. Studies assessing steroids (triamcinolone, dexamethasone and fluocinolone) have reported mixed results when compared with laser or placebo. Steroids have been associated with increased incidence of cataracts and intraocular pressure rise but require fewer injections, especially when steroid implants are used. The other treatment methods are by using: Primary prevention, Pathophysiology, Anti-VEGF, Corticosteroids. Intravitreal corticosteroids have potent anti-inflammatory effects. Triamcinolone (Kenalog) is not licensed for eye use but has been used to treat DMO for over 10 years. Triamcinolone (Trivaris) drug was recently accepted and started for eye use. Randomised controlled trials (RCT) were used to evaluate clinical effectiveness. Safety was assessed through both RCTs and observational studies. Ranibizumab (Lucentis, Genentech/Roche) is a fragment of the bevacizumab antibody (molecular weight of ranibizumab 48.4 KDa compared with 149 KDa for bevacizumab).