edema

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Related to alveolar edema: cardiac tamponade, pulmonary edema

edema

(ĭdē`mə), abnormal accumulation of fluid in the body tissues or in the body cavities causing swelling or distention of the affected parts. Edema of the ankles and lower legs (in ambulatory patients) is characteristic of congestive heart failure, but it can accompany other conditions, including obesity, diseased leg veins, kidney disease, cirrhosis of the liver, anemia, and severe malnutrition. Edema is the result of venous ulceration, which is often caused by an increase in tissue pressure (increased fluid within the tissue) because of increased capillary permeability. A failing heart is often accompanied by edema because the blood backs up into the veins, venules, and capillaries, thereby increasing blood pressure. In severe cases of heart failure, the abdomen may fill with fluid; this condition is called ascities. Appendage edema is often treated by bandaging the area to relieve pressure on the skin and decrease venous pressure. More severe cases may require a surgical procedure that diverts the blood flow to healthy veins. The accumulation of fluid within the lungs is a serious complication of cardiac failure, pneumonia, and other disorders. The collection of fluid in the pleural space (within the two-layered membrane surrounding the lungs) can be the symptom of numerous infectious and circulatory disorders. Lymphatic obstructions may result from various surgical procedures or from certain parasitic infections. These blockages cause increased back pressure in the lymph vessels and interfere with movement of fluid from interstitial tissue into venule ends of capillaries. The resulting collection of water within the skull is a serious and usually incurable condition (see hydrocephalushydrocephalus
, also known as water on the brain, developmental (congenital) or acquired condition in which there is an abnormal accumulation of body fluids within the skull. The congenital form may be associated with other abnormalities.
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). Since edema is a symptom, the underlying cause must be treated.

Edema

 

the excessive accumulation of fluid in the organs and intercellular tissue spaces of the body.

Edemas are classified according to the various conditions that can impair the drainage and retention of fluids. High pressure in the capillaries is the major factor in hydremic edemas. Hypoproteinemic edemas are primarily caused by a decrease in the amount of proteins, especially albumins, in the blood and by a drop in the colloidal osmotic, or oncotic, pressure of plasma, which is accompanied by a release of fluid from the capillary bed into the tissues. Membrane-related edemas result from increased capillary permeability owing to the effect of toxic and inflammatory processes and of disturbances of neural regulation in the capillary blood vessels.

Edema can be local—limited to a certain part of the body or organ—or general. Pronounced general edema is determined by inspection and palpation, after which a concavity remains in the edematous area. The condition is usually preceded by a substantial accumulation of fluid (about 4–9 liters) in the body. In persons suffering from heart disease (the commonest cause of hydremic edemas), edema is the most important symptom of cardiac insufficiency. It first arises in the feet and legs when the patient is standing and in the sacrum and lumbar region when the patient is lying down. These conditions then develop into total edema, or anasarca, of the subcutaneous tissue. Several conditions can arise if the fluid accumulates in the natural cavities of the body: hydrothorax is an accumulation in the pleural cavity; ascites, in the abdominal cavity; and hydropericardium, in the pericardial cavity.

Edema—chiefly hypoproteinemic—in the late stages of cirrhosis of the liver is usually combined with ascites and found mainly in the legs, lumbar region, and anterior abdominal wall. In kidney diseases, including nephritis, edema appears all over the body and face, where it is especially pronounced around the eyes. The edematous areas are soft to the touch and covered by pale skin. Salt and water retention in the kidneys, decreased concentration of proteins in the blood, and increased permeability of the vascular walls are major factors in the mechanism of the formation of these types of edema.

Aldosterone promotes fluid retention by causing the retention of sodium ions in the tissues. Thus, endocrine changes that result in the increased production of aldosterone play an important role in the origin of edema in diseases of the heart, kidneys, and liver. The production of the antidiuretic hormone vasopressin also increases in these diseases, resulting in increased reabsorption of water and salts in the renal tubules. Hormonal disturbances are the decisive factor in the development of edema in some endocrine disorders, for example, in Itsenko-Cushing syndrome. The edema observed after prolonged starvation is mainly hypoproteinemic.

Local edema in thrombophlebitis is caused by interference with the outflow of venous blood below the site of the thrombus. In such cases, the edema is firm, purple, painful to the touch, and covered with inflamed skin. When the outflow of lymph through the lymphatic system is disrupted, the surface edema on the limbs is firm, and the skin pale. Inflammatory edemas in such conditions as burns, furuncles, and erysipelas are due to increased capillary permeability and increased flow of blood into the inflamed area. The skin is reddish and painful to the touch.

Treatment of edemas is directed at the causative disease. Diuretics and special diets are prescribed.

REFERENCE

Eliseev, O. M. Oteki v klinike vnutrennikh boleznei. Moscow, 1970. (Bibliography.)

B. L. ELKONIN

edema

[ə′dē·mə]
(medicine)
An excessive accumulation of fluid in the cells, tissue spaces, or body cavities due to a disturbance in the fluid exchange mechanism. Also known as dropsy.

oedema

, edema
Pathol an excessive accumulation of serous fluid in the intercellular spaces of tissue
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Fourth, hypoxemia that due to ventilation-perfusion mismatch, intrapulmonary shunts, and an increased lung dead spaces, might result in the need for positive pressure ventilation.[33] Otherwise, the low oxygen or high carbon dioxide could downregulate the ENaC transcription and trafficking; in addition, the Na, K-ATPase functions are also impaired.[46],[47],[48] Therefore, supplemental oxygen and correction of hypercapnia might improve the resolution of alveolar edema.[46]
ALI and its more severe form ARDS are relatively common syndromes in critically ill patients, and are associated with high morbidity and mortality.[1] Pulmonary edema is a hallmark in ALI/ARDS and a life-threatening condition.[62],[101] It is widely accepted that resolution of alveolar edema is key for patient's survival.[2] Previously, clinical studies have shown that impaired alveolar fluid transport mechanisms contribute to the development, severity, and outcome of pulmonary edema in humans.[102] The AFC process is crucial to efficient gas exchange in the lung,[4] and ALI/ARDS patients with intact AFC have lower morbidity and mortality than those with compromised AFC.[32]
Alveolar edema must be cleared for the acute respiratory distress syndrome patient to survive.
The severity of lung injury was evaluated using a semi-quantitative histological index, as has been described previously.[sup][23] The histological index of lung damage included alveolar edema, hemorrhage, alveolar septal thickening and infiltration of polymorphonuclear leukocytes.
The amount of inflammatory cells infiltration and alveolar edema were reduced in the LPS + Ac-YVAD-CMK group when compared with the LPS + Z-DEVD-FMK group.
The exudative phase is characterized by hyaline membranes, interstitial and alveolar edema, alveolar capillary congestion, intracapillary neutrophil margination, interstitial inflammation, and microvascular thromboemboli.
In summary, they found that anti-IL-8:IL-8 complexes purified from alveolar edema fluids from patients with ALI have the capacity to trigger an inflammatory response in the lung by attracting and activating human blood neutrophils, strongly suggesting that anti-IL-8:IL-8 complexes are involved in ALI/ARDS pathogenesis.
The LUS image can be simplified as follows: The normal lung is "black," the moderately diseased lung (with interstitial water) is "black and white" (with white lines corresponding to B-lines), and the markedly diseased lung (with alveolar edema) is "white" (diffusely bright).
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) often occur in severe diseases such as serious infection, shock, trauma, and burn, and are clinically characterized by progressive hypoxemia and respiratory distress syndrome, contributing to diffuse pulmonary interstitial and alveolar edema caused by pulmonary capillary endothelial cells and alveolar epithelial cell injury.
Histopathology showed more alveolar edema, hemorrhage, wall thickening and hyperinflation, and infiltration of significant numbers of inflammatory cells into the alveolar spaces and interstitial spaces in the LPS group.
There was intense alveolar edema in both lower lobes.