Edema of unknown cause occurs primarily in women. Varicose veins or thrombophlebitis (a blood clot in an inflamed vein) of the deep veins in the legs causes edema that is localized to the legs.
Therapy for edema consists of treating the underlying conditions, restricting salt intake, and often using diuretics (medicines to induce urination).
What is edema?
Edema is observable swelling from fluid accumulation in body tissues. Edema most commonly occurs in the feet and legs, where it is referred to as peripheral edema. The swelling is the result of the accumulation of excess fluid under the skin in the spaces within the tissues. All tissues of the body are made up of cells and connective tissues that hold the cells together. This connective tissue around the cells and blood vessels is known as the interstitium. Most of the body's fluids that are found outside of the cells are normally stored in two spaces; the blood vessels (as the "liquid" or serum portion of your blood) and the interstitial spaces (not within the cells). In various diseases, excess fluid can accumulate in either one or both of these compartments.
The body's organs have interstitial spaces where fluid can accumulate. An accumulation of fluid in the interstitial air spaces (alveoli) in the lungs occurs in a disorder called pulmonary edema. In addition, excess fluid sometimes collects in what is called the third space, which includes cavities in the abdomen (abdominal or peritoneal cavity - called "ascites") or in the chest (lung or pleural cavity - called "pleural effusion"). Anasarca refers to the severe, widespread accumulation of fluid in the all of the tissues and cavities of the body at the same time.
What is pitting edema and how does it differ from non-pitting edema?
Pitting edema can be demonstrated by applying pressure to the swollen area by depressing the skin with a finger. If the pressing causes an indentation that persists for some time after the release of the pressure, the edema is referred to as pitting edema. Any form of pressure, such as from the elastic in socks, can induce pitting with this type of edema. This type of edema may be normal depending on the severity. Almost everyone wears socks all day will have mild pitting edema by the end of the day.
In non-pitting edema, which usually affects the legs or arms, pressure that is applied to the skin does not result in a persistent indentation. Non-pitting edema can occur in certain disorders of the lymphatic system such as lymphedema, which is a disturbance of the lymphatic circulation that may occur after a mastectomy, lymph node surgery, or congenitally. Another cause of non-pitting edema of the legs is called pretibial myxedema, which is a swelling over the shin that occurs in some patients with hypothyroidism. Non-pitting edema of the legs is difficult to treat. Diuretic medications are generally not effective, although elevation of the legs periodically during the day and compressive devices may reduce the swelling.
What causes pitting edema?
Edema is caused by either systemic diseases, that is, diseases that affect the various organ systems of the body, or by local conditions involving just the affected extremities. The most common systemic diseases associated with edema involve the heart, liver, and kidneys. In these diseases, edema occurs primarily because of the body's retention of too much salt (sodium chloride). The excess salt causes the body to retain water. This water then leaks into the interstitial tissue spaces, where it appears as edema.
How does salt intake affect edema?
The body's balance of salt is usually well-regulated. A normal person can consume small or large quantities of salt in the diet without concern for developing salt depletion or retention. The intake of salt is determined by dietary patterns and the removal of salt from the body is accomplished by the kidneys. The kidneys have a great capacity to control the amount of salt in the body by changing the amount of salt eliminated (excreted) in the urine. The amount of salt excreted by the kidneys is regulated by hormonal and physical factors that signal whether retention or removal of salt by the kidneys is necessary.
If the blood flow to the kidneys is decreased by an underlying condition such as heart failure, the kidneys react by retaining salt. This salt retention occurs because the kidneys perceive that the body needs more fluid to compensate for the decreased blood flow. If the patient has a kidney disease that impairs the function of the kidneys, the ability to excrete salt in the urine is limited. In both conditions, the amount of salt in the body increases, which causes the patient to retain water and develop edema.
Patients experiencing a disturbance in their ability to normally excrete salt may need to either be placed on a diet limited in salt and/or given diuretic medications (water pills). In the past, patients with diseases associated with edema were placed on diets very restricted in salt intake. With the development of new and very potent diuretic agents, this marked restriction in dietary salt intake is generally no longer necessary. These diuretics work by blocking the reabsorption and retention of salt by the kidneys, thereby increasing the amount of salt and water that is eliminated in the urine.
Why does a patient with heart disease retain fluid?
Heart failure is the result of poor cardiac function and is reflected by a decreased volume of blood pumped out by the heart, called cardiac output. Heart failure can be caused by weakness of the heart muscle, which pumps blood out through the arteries to the entire body, or by dysfunction of the heart valves, which regulate the flow of blood between the chambers of the heart. The diminished volume of blood pumped out by the heart (decreased cardiac output) is responsible for a decreased flow of blood to the kidneys. As a result, the kidneys sense that there is a reduction of the blood volume in the body. To counter the seeming loss of fluid, the kidneys retain salt and water. In this instance, the kidneys are fooled into thinking that the body needs to retain more fluid volume when, in fact, the body already is holding too much fluid.
This fluid increase ultimately results in the buildup of fluid within the lungs, which causes shortness of breath. Because of the decreased volume of blood pumped out by the heart (decreased cardiac output), the volume of blood in the arteries is also decreased, despite the actual increase in the body's total fluid volume. An associated increase in the amount of fluid in the blood vessels of the lungs causes shortness of breath because the excess fluid from the lungs' blood vessels leaks into the airspaces (alveoli) and interstitium in the lungs. This accumulation of fluid in the lung is called pulmonary edema. At the same time, accumulation of fluid in the legs causes pitting edema. This edema occurs because the build-up of blood in the veins of the legs causes leakage of fluid from the legs' capillaries (tiny blood vessels) into the interstitial spaces.
An understanding of how the heart and lungs interact will help you to better comprehend how fluid retention works in heart failure. The heart has four chambers; an atrium and a ventricle on the left side of the heart and an atrium and ventricle on the right. The left atrium receives oxygenated blood from the lungs and transfers it to the left ventricle, which then pumps it through the arteries to the entire body. The blood then is transported back to the heart by veins into the right ventricle and transferred to the right ventricle, which then pumps it to the lungs for re-oxygenation.
Left-sided heart failure, which is due primarily to a weak left ventricle, usually is caused by coronary artery disease, hypertension, or disease of the heart valves. Typically, when these patients initially come to the doctor they are troubled by shortness of breath with exertion and when lying down at night (orthopnea). These symptoms are due to pulmonary edema that is caused by pooling of the blood in the vessels of the lungs.
In contrast, right-sided heart failure, which often is due to obstructive sleep apnea or chronic lung diseases such as emphysema, initially causes salt retention and edema. Persistent salt retention in these patients, however, may lead to an expanded blood volume in the blood vessels, thereby causing fluid accumulation in the lungs (pulmonary congestion) and shortness of breath.
In patients with heart failure due to weak heart muscle (cardiomyopathy), both the right and left ventricles of the heart are usually affected. These patients, therefore, can initially suffer from swelling both in the lungs (pulmonary edema) and in the legs and feet (peripheral edema). The physician examining a patient who has congestive heart failure with fluid retention looks for certain signs. These include:
Pitting edema of the legs and feet
Rales in the lungs (moist crackle sounds from the excess fluid that can be heard with a stethoscope)
A gallop rhythm (three heart sounds instead of the normal two due to muscle weakness)
Distended neck veins. The distended neck veins reflect the accumulation of blood in the veins that are returning blood to the heart
Why do patients with liver disease develop ascites and edema?
In patients with chronic diseases of the liver, fibrosis (scarring) of the liver often occurs. When the scarring becomes advanced, the condition is called cirrhosis of the liver. Ascites is excessive fluid that accumulates in the abdominal (peritoneal) cavity. It is a complication of cirrhosis and appears as an abdominal bulge. The peritoneum is the inner lining of the abdominal cavity, which also folds over to cover the organs inside the abdomen such as the liver, gallbladder, spleen, pancreas, and intestines. Ascites develops because of a combination of two factors:
Increased pressure in the vein system that carries blood from the stomach, intestines, and spleen to the liver (portal hypertension)
A low level of the protein albumin in the blood (hypoalbuminemia). Albumin, which is the predominant protein in the blood and which helps maintain blood volume, is reduced in cirrhosis primarily because the damaged liver is not able to produce enough of it.
Other consequences of portal hypertension include dilated veins in the esophagus (varices), prominent veins on the abdomen, and an enlarged spleen. Each of these conditions is due primarily to the increased pressure and accumulation of blood and excess fluid in the abdominal blood vessels. The fluid of ascites can be removed from the abdominal cavity by using a syringe and a long needle, a procedure called paracentesis. Analysis of the fluid can help differentiate ascites that is caused by cirrhosis from other causes of ascites, such as cancer, tuberculosis, congestive heart failure, and nephrosis. Sometimes, when ascites does not respond to treatment with diuretics, paracentesis can be used to remove large amounts of the ascitic fluid.
Peripheral edema, which is usually seen as pitting edema of the legs and feet, also occurs in cirrhosis. The edema is a consequence of the hypoalbuminemia and the kidneys retaining salt and water.
The presence or absence of edema in patients with cirrhosis and ascites is an important consideration in the treatment of the ascites. In patients with ascites without edema, diuretics must be given with extra caution. Diuresis (induced increased volume of urine by use of diuretics) that is too aggressive or rapid in these patients can lead to a low blood volume (hypovolemia), which can causekidney and liver failure. In contrast, when patients who have both edema and ascites undergo diuresis, the edema fluid in the interstitial space serves as somewhat of a buffer against the development of low blood volume. The excess interstitial fluid moves into the blood vessel spaces to rapidly replenish the depleted blood volume.
Why does edema occur in patients with kidney disease?
Edema forms in patients with kidney disease for two reasons:
A heavy loss of protein in the urine
Impaired kidney (renal) function
Heavy loss of protein in the urine
In this situation, the patients have normal or fairly normal kidney function. The heavy loss of protein in the urine (over 3.0 grams per day) with its accompanying edema is termed the nephrotic syndrome. Nephrotic syndrome results in a reduction in the concentration of albumin in the blood (hypoalbuminemia). Since albumin helps to maintain blood volume in the blood vessels, a reduction of fluid in the blood vessels occurs. The kidneys then register that there is depletion of blood volume and, therefore, attempt to retain salt. Consequently, fluid moves into the interstitial spaces, thereby causing pitting edema.
The treatment of fluid retention in these patients is to reduce the loss of protein into the urine and to restrict salt in the diet. The loss of protein in the urine may be reduced by the use of ACE inhibitors and angiotensin receptor blockers (ARB's). Both categories of drugs, which ordinarily are used to lower blood pressure, prompt the kidneys to reduce the loss of protein into the urine.
ACE inhibitor drugs include:
enalapril (Vasotec),
quinapril (Accupril),
captopril (Capoten),
benazepril (Lotensin),
trandolapril (Mavik),
lisinopril (Zestril or Prinivil), and
ramipril (Altace).
Angiotensin receptor blockers include:
losartan (Cozaar),
valsartan (Diovan),
candesartan (Atacand), and
irbesartan (Avapro).
Certain kidney diseases may contribute to the loss of protein in the urine and the development of edema. A biopsy of the kidney may be needed to make a diagnosis of the type of kidney disease, so that treatment may be given.
Impaired kidney (renal) function
In this situation, patients who have kidney diseases that impair renal function develop edema because of a limitation in the kidneys' ability to excrete sodium into the urine. Thus, patients with kidney failure from whatever cause will develop edema if their intake of sodium exceeds the ability of their kidneys to excrete the sodium. The more advanced the kidney failure, the greater the problem of salt retention is likely to become. The most severe situation is the patient with end-stage kidney failure who requires dialysis therapy. This patient's salt balance is totally regulated by dialysis, which can remove salt during the treatment. Dialysis is a method of cleansing the body of the impurities that accumulate when the kidneys fail. Dialysis is accomplished by circulating the patient's blood over an artificial membrane (hemodialysis) or by using the patient's own abdominal cavity (peritoneal membrane) as the cleansing surface. Individuals whose kidney function declines to less than 5% to 10% of normal may require dialysis.
Which diuretics are used to treat edema?
Edema can become a problem in systemic diseases of the heart, liver or kidneys. Diuretic therapy can be initiated, often alleviating the edema. The most potent diuretics are loop diuretics, so-called because they work in the portion of the kidney tubules referred to as the loop of Henle. The kidney tubules are small ducts that regulate salt and water balance, while transporting the forming urine. Clinical loop diuretics available are:
furosemide (Lasix),
torsemide (Demadex), and
butethamine (Bumex).
The doses of these diuretics vary depending upon the clinical circumstances. These drugs can be given orally, although seriously ill patients in the hospital may receive them intravenously for more prompt or effective response. If one of the loop diuretics is not effective alone, it may be combined with an agent that works further down (more distally) in the tubule. These agents include the thiazide type diuretics, such as hydrochlorothiazide (HydroDIURIL), or a similar but more potent type of diuretic called metolazone (Zaroxolyn). When diuretics that work at different sites in the kidney are used together, the response often is greater than the combined responses to the individual diuretics (synergistic response).
Some diuretics frequently cause an excessive loss of potassium in the urine, leading to the depletion of body potassium. These drugs include the loop diuretics, the thiazide diuretics, and metolazone. Patients on these diuretics are commonly advised to take potassium supplements and/or to eat foods high in potassium. High potassium foods include certain fruits such as:
Bananas
Orange juice
Tomatoes
Potatoes
Patients with impaired kidney function often do not require potassium supplements with diuretics because their damaged kidneys tend to retain potassium. In certain instances, the volume of urine induced by the diuretic can be improved by adding a potassium-sparing diuretic, one that does not cause depletion of potassium. These diuretics include spironolactone (Aldactone), triamterene (Dyrenium, a component of Dyazide), and amiloride (Midamor). Adding one of these diuretics to the patient's diuretic regimen may preclude the need for potassium supplements. Another diuretic that can be used is acetazolamide (Diamox), which counteracts the development of an increased concentration of bicarbonate (too much alkali) in the blood. Increased bicarbonate sometimes occurs in patients receiving other diuretics.
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