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Edema -General Aspects

This lecture on edema simplifies the concept of development of edema along with related causes and aspects.

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Outline of Lecture


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.

Pathophysiology of edema formation

There are two basic steps involved in edema formation:

  • An alteration in capillary hemodynamics that favors the movement of fluid from the vascular space into the interstitium.
  • The retention of dietary or intravenously administered sodium and water by the kidneys.

Capillary hemodynamics

The exchange of fluid between the plasma and the interstitium is determined by the hydraulic and oncotic pressures in each compartment.

The relationship between these parameters can be expressed by Starling’s law.

Starling’s law

Capillary hydrostatic pressure

Interstitial hydrostatic pressure

Capillary oncotic pressure

Interstitial oncotic pressure

Net filtration  =

Lp S   x   (Δ hydraulic P – Δ oncotic P)

Lp is the unit permeability of the capillary wall

S is the surface area available for fluid movement

Δ hydraulic P = P capillaries  – P interstitial fluid

Δ oncotic P =  O capillaries  – O interstitial fluid

Renal sodium retention


As noted above, the retention of fluid by the kidney in edematous states can represent :

  • An appropriate compensatory response to effective arterial or circulating volume depletion
  • An inappropriate manifestation of renal disease.

Major causes of edema according to primary mechanism

Increased capillary hydraulic pressure

A. Increased plasma volume due to renal Na+ retention

1. Heart failure, including cor pulmonale

2. Primary renal sodium retention

a.Renal disease, including the nephrotic syndrome

b. Drugs: calcium channel blockers, NSAIDs, fludrocortisone, estrogens

c. Refeeding edema

3. Pregnancy and premenstrual edema

B. Venous obstruction

1. Cirrhosis or hepatic venous obstruction

2. Acute pulmonary edema

3. Local venous obstruction

C. Decreased arteriolar resistance

  • Calcium channel blockers (?)
  • Idiopathic edema (?)


A. Protein loss

1. Nephrotic syndrome

2. Protein-losing enteropathy

B. Reduced albumin synthesis

1. Liver disease

2. Malnutrition

Increased capillary permeability

A. Idiopathic edema

B. Burns

C. Trauma

D. Inflammation or sepsis

E. Allergic reactions, including certain forms of angioedema

F. Adult respiratory distress syndrome

G. Diabetes mellitus

H. Malignant ascites

Lymphatic obstruction or increased interstitial oncotic pressure

A. Lymph node dissection

B. Nodal enlargement due to malignancy

C. Hypothyroidism

D. Malignant ascites


The most common causes of generalized edema seen by the clinician are:

  • Heart failure
  • Cirrhosis
  • Nephrotic syndrome and other forms of renal disease
  • Premenstrual edema and pregnancy

Heart failure

The edema in the different causes of heart failure is due to an increase in venous pressure that produces a parallel rise in capillary hydraulic pressure.

Pure left heart failure typically present with pulmonary but not peripheral edema.

Pure right ventricular failure results in prominent edema in the lower extremities and perhaps ascites.

Both right and left ventricle failure often leads to the simultaneous onset of pulmonary and peripheral edema.


The development of portal hypertension is the first step toward fluid retention in the setting of cirrhosis.

Patients with cirrhosis and ascites usually have a marked reduction in systemic vascular resistance and in mean arterial pressure plus an increase in cardiac output.

The retention of sodium and water increases the plasma volume.

Nephrotic syndrome

Two major factors have been thought to be responsible for this problem and it is likely that both contribute to a variable degree in individual patients:

  • Arterial underfilling as the low plasma oncotic pressure leads to plasma volume depletion
  • Sodium retention directly induced by the renal disease



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