Abstract
With the exception of those clinical situations in which edema is due primarily to local phenomena (such as obstruction to venous flow from a thrombus or inflammatory reaction due to infection), the final common pathway by which edema fluid is formed involves the retention of salt (and water) by the kidney. Thus, whether the kidney is responding in a manner which will be beneficial to the patient’s welfare (as in the case of hypovolemic shock) or inimical to the patient’s best interests (as in congestive heart failure), this response to preserve body volume results from what is perceived by the kidney to be a reduction in vascular filling in the arterial circuit. Accordingly, as will be spelled out in detail below, the first consideration in the therapy of the edema state involves correction of the underlying disorder, if that is possible. In those cases in which the deranged physiology cannot be reversed, the mainstays of therapy are the institution of a reduction in the salt content of the diet and the administration of diuretic agents. The diuretics currently available have in common the capacity to impair sodium chloride and/or sodium bicarbonate reabsorption at one or more site or sites along the tubular system, and are basically of three types: 1) Those agents, like the thiazide group, which are moderately natriuretic and are therefore given to treat mild to moderate edema. 2) Drugs such as furosemide which are more potent, and are therefore administered in cases of more severe or even ‘resistant’ edema. 3) Finally, a group of special purpose agents such as spironolactone and triamterene, prescribed not so much for natriuretic potency (which is small), but because of their ability to suppress potassium secretion into the tubular lumen. When diuretic drugs are utilized, the physician would do well to remember that, as with all other classes of agents, there is a price to be paid in terms of side effects encountered for each of the drugs employed. Furthermore, in general it is true that the more potent the diuretic, the greater the potential for encountering these adverse effects and the more severe they are likely to be.
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Puschett, J.B., Greenberg, A. (1984). Treatment of Edematous States. In: Suki, W.N., Massry, S.G. (eds) Therapy of Renal Diseases and Related Disorders. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-3807-9_3
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