Idiopathic Edema

Idiopathic edema is a disorder characterized by fluid retention that cannot be attributed to the known causes or the pathogenic mechanisms of edema formation listed earlier. Although the etiology of this syndrome has not been clarified yet, it is clear that idiopathic edema overwhelmingly occurs in women. It is important to distinguish this disorder from excessive estrogen-stimulated sodium and fluid retention associated with the premenstrual state (cyclic or premenstrual edema). True idiopathic edema has been reported in postmenopausal women, and episodes of fluid retention bear no relationship to the menstrual cycle. In most series of patients, other edema-forming states such as cardiac, renal, or hepatic disease have been excluded. It is therefore likely that idiopathic edema is not a single entity, but rather the result of multiple etiologies [8].

An important consistent finding in idiopathic edema is the observation that most of the affected patients retain sodium and water in the upright posture, but diurese in the recumbent position. There is evidence to suggest that decreased plasma volume with concomitant increase in plasma renin and aldosterone activity are frequent findings. The relative importance of secondary hyperaldosteronism in sustaining the progressive fluid gain in this disorder is highlighted by the observation that treatment with angiotensin-converting enzyme inhibitors often results in fluid loss and symptomatic improvement.

The possibility that an underlying abnormality exists in capillary permeability leading to loss of intravascular volume in the upright posture has also been considered. Studies provided evidence showing a decrease in plasma volume and increased disappearance rates of albumin from the plasma. Some studies have suggested an increase in edema fluid protein concentrations, and others have reported increased catabolic rates for serum albumin. Although severe hypoalbuminemia is not a feature of the disorder, small decreases in serum albumin concentration have been noted. The mechanisms underlying the increased permeability of the capillaries are poorly understood. However, it was shown that IL-2 may have a major role in the pathogenesis of this syndrome. It was also suggested that some patients with idiopathic edema are, or have been, diuretic users. Because diuretic agents induce a degree of volume depletion, many of the mechanisms controlling sodium excretion are stimulated to compensate for the natriuresis. This "braking" phenomenon provides patients a new steady state of external sodium balance. Thus, proximal fluid reabsorption might increase and the renin-angiotensin-aldosterone system would be overstimulated.

In summary, idiopathic edema may be the end result of multiple etiologies. After exclusion of certain metabolic and other edema-forming states, it is likely that certain forms exist in which primary disturbances in capillary permeability result in decreased circulating plasma volume.


Colloid osmotic pressure: The effective pressure between the plasma and the interstitial compartment provided by osmotically active particles (proteins) that do not pass the freely between semi-permeable membranes.

Extracellular fluid: The fluid contained in the plasma and the interstitial compartment.

Hydraulic pressure: The hydrostatic pressure formed within the intravascular compartment.

Microvascular permeability: Alterations in the vascular permeability of the microcirculation.

Starling equation: Provides the calculation of forces driving fluid movement across the capillaries.


1. Peters, J. P. (1948). The role of sodium in the production of edema. N. Engl. J. Med. 239, 353-362.

2. Michel, C. C. (1997). Starling: The formulation of his hypothesis of microvascular fluid exchange and its significance after 100 years. Exp. Physiol. 82(1), 1-30. This review article emphasizes the important contribution of Starling to the understanding of the main mechanisms of edema formation.

3. Kumar, V., Cortan, R. S., and Robbins, S. L. (2003). Basic Pathology, 7th ed. Philadelphia: W. B. Saunders.

4. Abbas, A. K., Lichtman, A. H., and Pober, J. S. (2000). Cellular and Molecular Immunology, 4th ed. Philadelphia: W.B. Saunders.

5. Schrier, R. W. (1988). Pathogenesis of sodium and water retention in high-output and low-output cardiac failure, nephrotic syndrome, cirrhosis, and pregnancy. N. Engl. J. Med. 319(16), 1065-1072. An excellent review on the pathogenesis of edema formation in clinical practice.

6. Schrier, R. W., and Abraham, W. T. (1999). Hormones and hemody-namics in heart failure. N. Engl. J. Med. 341(8), 577-585.

7. Kaufman, D. R., and Choi, Y. (1999). Signaling by TNF receptors: Pathways, paradigms and targets for therapeutic modulation. Int. Rev. Immunol. 18(4), 405-427. A comprehensive review on proinflammatory cytokines involved in edema formation.

8. Streeten, D. H. (1995). Idiopathic edema. Pathogenesis, clinical features, and treatment. In: Endocrinology and Metabolism Clinics of North America, R. G. Dluhy, ed., Philadelphia: W. B. Saunders.

Capsule Biography

Dr. Hershko is a Senior Surgeon in the Department of Surgery A at the Rambam Medical Center in Haifa, Israel. His main research interests are the regulation of proinflammatory cytokines in sepsis and the role of cell-cycle regulatory proteins in cancer progression. He has received the Israel Cancer Research Fund (ICRF) Career Development Award.

Dr. Krausz has headed the Department of Surgery A at the Rambam Medical Center in Haifa, Israel, since 1996. His main research interests are fluid treatment of trauma casualties in civilian as well as military scenarios, and lately his research has also focused on gender differences in hemor-rhagic as well as septic shock, and the role of leukocytes in pathophysiol-ogy of these phenomena. He has received grants from the Israel Academy of Sciences and the Israeli Ministry of Health.

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