Edema in childhood

Edema in childhood. There are two types of edema: localized edema and generalized edema. The causes of generalized edema in childhood are diverse. Formation of generalized edema involves retention of sodium and water in the kidney. The treatment of generalized edema depends on the primary etiology. Supportive nutritional and medical therapies are needed to prevent further edema. These and related features of edema in childhood are discussed in this review. Edema can be defined as the presence of excess fluid in the interstitial space of the body. Edema is divided into two types, localized edema and generalized edema. The formation of edema is associated with renal sodium retention. However, localized edema does not reflect a sustained impairment in the ability to maintain normal sodium balance. Generalized edema can arise via two different processes: (1) a reduced intravascular volume leading to sodium and water retention, that is, an "underfilling edema," or (2) sodium and water retention secondary to ex­ panded plasma and intracellular tissue fluid volume accompanied by a lack of natriuresis, that is, an "overfilling edema" (1). The generalized edema occurs in the presence of parenchymal renal damage (nephrotic syndrome, acute and chronic glomerulone­ phritis and renal failure) or in the absence of structural renal disease (heart failure, liver cirrhosis). Idiopathic edema affects women in the menstrual period or in the immediate premenstrual period, who manifest generalized edema secondary to water and sodium retention (2). Idiopathic edema is uncommon in the pediatric age group. Toxemia of pregnancy is characterized by generalized edema and hypertension (1), The severity of renal involvement is correlated to the degree of proteinuria. A less easily classified type of edema is the edema of seques­ tration {third space}, which is associated with contracted extra­ cellular volume for which the treatment is distinctly different, requiring infusion of extracellular-like osmotic colloids (3), The mechanism of "underfilling edema" is initiated with an increased glomerular permeability to albumin, that is, albumin­ uria. The subsequent hypoalbuminemia leads to decreased plasma oncotic pressure accompanied by movement of water from intra­ vascular space to the interstitium. The intravascular contracted volume in turn stimulates the following neuroendocrinological factors, resulting in sodium and water retention: (1) an increased renin-angiotensin-aldosterone (RAA) activity; (2) an increased