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Le hablas de tabaquismo HOY o le hablas de enfermedad mañana.


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General Principles of the Treatment of Edema in Adults http://www.scribd.com/doc/24870246/General-Principles-of-the-Treatme...

General principles of the treatment of edema in adults

Author
Burton D Rose, MD
Section Editor
Robert H Fletcher, MD,
MSc Deputy Editor
David M Rind, MD

Last literature review version 17.2: Maio 2009 | This topic last updated:
Junho 11, 2009 (More)

INTRODUCTION — Edema is defined as a palpable swelling produced by


expansion of the interstitial fluid volume; when massive and generalized, the
excess fluid accumulation is called anasarca. A variety of clinical conditions are
associated with the development of edema, including heart failure, cirrhosis, and
the nephrotic syndrome, as well as local conditions such as venous and lymphatic
disease (show table 1). (See "Pathophysiology and etiology of edema in adults").

The general principles the treatment of edema in adults, including the use of
diuretics to remove the excess fluid, will be reviewed here. The specific effects of
diuretics in the three major generalized edema states (heart failure, cirrhosis, and
the nephrotic syndrome) is discussed in greater detail in the appropriate topic
reviews. (See "Use of diuretics in heart failure" and see "Initial therapy of ascites in
patients with cirrhosis", section on Diuretic therapy, and see "Mechanism and
treatment of edema in nephrotic syndrome").

The clinical features and diagnosis of generalized edematous states, the treatment
of refractory edema, and the approach to edema in children are discussed
separately. (See "Clinical manifestations and diagnosis of edema in adults" and see
"Treatment of refractory edema" and see "Evaluation and management of edema in
children").

GENERAL PRINCIPLES OF THERAPY — Treatment of edema consists of reversal


of the underlying disorder (if possible), dietary sodium restriction (to minimize fluid
retention), and, in most patients, diuretic therapy. Before initiating the use of
diuretics, it is important to consider the following questions, which apply to all
edematous states:

• When must edema be treated?


• What are the consequences of the removal of edema fluid?

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Explore Content

Loop Diuretics Adult Patient Diuretic Therapy Fluid Removal

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• How rapidly should edema fluid be removed?

When must edema be treated? — Pulmonary edema is the only form of


generalized edema that is life-threatening and requires immediate treatment. (See
"Treatment of acute decompensated heart failure", section on Diuretics).

In all other edematous states, the removal of the excess fluid can proceed more
slowly, since it is of no danger to the patient. This is particularly true in patients
with cirrhosis in whom hypokalemia, metabolic alkalosis, and rapid fluid shifts
induced by diuretics can precipitate hepatic coma or the hepatorenal syndrome.
(See "Initial therapy of ascites in patients with cirrhosis", section on Diuretic
therapy).

What are the consequences of the removal of edema fluid? — The retention
of sodium and water by the kidney in heart failure and cirrhosis is compensatory in
that it acts to raise the effective circulating volume toward normal. In comparison,
fluid accumulation is inappropriate with primary renal sodium retention, where the
effective circulating volume as well as the total extracellular volume are expanded.
(See "Pathophysiology and etiology of edema in adults").

When the retention of edema fluid is compensatory, then removal of this fluid with
diuretics should diminish the effective circulating volume. To the degree that the
fluid lost by diuresis comes from the plasma volume, there will be a decrease in
venous return to the heart and therefore in the cardiac filling pressures. From the
Frank-Starling relationship, this reduction in the left ventricular end-diastolic filling
pressure (LVEDP) should lower the stroke volume in both normal and failing hearts,
possibly resulting in a fall in cardiac output and consequently in tissue perfusion.

There is a large body of evidence that this sequence occurs commonly in


edematous states. First, the administration of diuretics to patients with either acute
or chronic heart failure frequently leads to a reduction in cardiac output [1-3]. A
similar sequence can occur in cirrhosis, particularly in patients who are rapidly
diuresed [4,5]. Second, diuretic-induced fluid removal leads to increased secretion
of the three "hypovolemic" hormones (renin, norepinephrine, and ADH) in many
patients with heart failure or cirrhosis [6-8]. (See "Use of diuretics in heart failure",
section on Hemodynamic consequences of the diuresis, and see "Initial therapy of
ascites in patients with cirrhosis", section on Overly rapid fluid removal).

Despite the reduction that may occur in the effective circulating volume, most
patients benefit from the appropriate use of diuretics. As an example, the
diminished exercise tolerance and symptoms of pulmonary congestion in patients

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with heart failure are often improved by diuretic therapy, even though the cardiac
output may fall by an average of 20 percent [2]. This observation suggests that
small reductions in the cardiac output can be well tolerated. Similarly, relief of
symptoms of fatigue and bloating are common in patients with noncardiac causes
of edema.

However, the decrease in the effective circulating volume is sufficient to


significantly impair tissue perfusion in selected patients. This most often occurs in
two settings: when there is a low baseline effective circulating volume, as in severe
heart failure; and after overly rapid fluid removal [4].

The adequacy of tissue perfusion can be estimated simply by monitoring the BUN
and plasma creatinine concentration. As long as these parameters remain constant,
it can be assumed that diuretic therapy has not led to a significant impairment in
perfusion to the kidney or, therefore, to other organs. In comparison, significant
elevations in the BUN and plasma creatinine concentration indicate that further fluid
removal should be avoided and that other therapeutic measures should be
attempted (such as vasodilator or inotropic therapy in heart failure). The decline in
tissue perfusion in this setting can also lead to weakness, fatigue, postural
dizziness, and lethargy and confusion due to decreased cerebral blood flow. (See
"Use of diuretics in heart failure", section on Hemodynamic consequences of the
diuresis).

In contrast to the adverse hemodynamic changes that may be seen in heart failure,
cirrhosis, or some cases of the nephrotic syndrome, impaired renal perfusion should
not occur after the appropriate use of diuretics in patients with primary renal
sodium retention (show table 1). In these conditions, the effective circulating
volume is increased by fluid retention. Although diuretics reduce the effective
circulating volume, it will be from an initially high level back toward normal.

How rapidly should edema fluid be removed? — When diuretics are


administered, the fluid that is lost initially comes from the intravascular space. This
results in a reduction in the venous pressure and consequently in capillary hydraulic
pressure, thereby promoting restoration of the plasma volume by the mobilization
of edema fluid into the vascular space. The rapidity with which this occurs is
variable. In patients with generalized edema due to heart failure, the nephrotic
syndrome, or primary sodium retention, the edema fluid can be mobilized rapidly,
since most capillary beds are involved. Thus, removal of 2 to 3 liters of edema fluid
or more in 24 hours can usually be accomplished in patients with anasarca without
a clinically significant reduction in plasma volume.

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One important exception occurs with cirrhosis and ascites, but no peripheral edema
[4,5]. In this setting, the excess ascitic fluid can only be mobilized via the
peritoneal capillaries. Direct measurements have indicated that 300 to 500 mL/day
is the maximum level that can be mobilized by most patients [4,5,8]. If the diuresis
proceeds more rapidly, the ascitic fluid will be unable to completely replenish the
plasma volume (show figure 1), resulting in azotemia and possible precipitation of
the hepatorenal syndrome. This limitation does not apply to patients who also have
peripheral edema, since the rate of fluid mobilization is relatively unlimited in this
setting (show figure 1). (See "Initial therapy of ascites in patients with cirrhosis",
section on Overly rapid fluid removal).

Venous insufficiency and lymphedema — Patients with localized edema due to


venous or lymphatic obstruction represent another setting in which diuretic therapy
will lead to volume depletion. As discussed above, a reduction in venous and
therefore intracapillary pressure with fluid removal in a patient with edema allows
the edema fluid to be mobilized and the plasma volume to be maintained. However,
this sequence will not occur in patients with venous insufficiency, moderate to
severe lymphedema, or ascites due to peritoneal malignancy [9]. As a result,
diuretics should be used with caution in such patients. (See "Lymphedema:
Prevention and treatment", section on Diuretics).

The mainstays of therapy of lower extremity edema due to venous insufficiency are
leg elevation and well-fitted, knee-high compression stockings. Some medical
therapies also may be effective. These modalities are discussed in detail elsewhere.
(See "Medical management of lower extremity chronic venous disease").

Lymphedema is also difficult to treat in many patients. (See "Lymphedema:


Prevention and treatment").

USE OF DIURETICS — Diuretic therapy in generalized edematous states is


generally begun with a loop diuretic such as furosemide. In addition to monitoring
the degree of diuresis, patients should also be monitored for fluid and electrolyte
complications such as hypokalemia, metabolic alkalosis, hyponatremia, and
hyperuricemia.

The approach to therapy has some unique features in each of the generalized
edematous states:

• For patients with cirrhosis, spir o no lacto ne and a loop diuretic is the preferred
initial regimen. The diuresis should proceed slowly in the absence of edema,
and patients with tense ascites are often treated with total paracentesis.

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