Why does edema develop?
Edema develops because of a perturbation in the Starling forces that govern the distribution of fluid between the vascular and the interstitial compartments.
• In primary kidney sodium retention, there is overfilling of the vascular compartment. This leads to increased venous pressure and increased capillary hydraulic pressure. Capillary hydraulic pressure is one of the Starling forces; increased capillary hydraulic pressure favors movement of fluid into the interstitium. Continued kidney retention of ingested sodium and water augments this process.
• In CHF, there is also overfilling of the vascular compartment, increased venous pressure, and increased capillary hydraulic pressure, which favors movement of fluid into the interstitium. Although there is overfilling of the vascular compartment, effective arterial volume is low. In other words, vascular underfilling is sensed. Avid kidney reabsorption of ingested sodium and water serves to increase effective arterial volume and increase effective tissue perfusion—but also augments edema formation.
• In cirrhosis, splanchnic vasodilatation is an early phenomenon. Sinusoidal obstruction in the cirrhotic liver leads to an increase in the hydraulic pressure in the sinusoids. Fluid in the sinusoids moves across the hepatic capsule into the peritoneum. Ascites formation and splanchnic vasodilatation lead to a state of low effective arterial volume. Low effective arterial volume leads to avid reabsorption of ingested sodium and water, which augments ascites formation.
• In nephrotic syndrome, two mechanisms of edema formation (to varying degrees in individual patients) may be operative. Primary kidney sodium retention may lead to increased capillary hydraulic pressure and movement of fluid into the interstitium. Alternatively, low plasma oncotic pressure from hypoalbuminemia may lead to movement of fluid into the interstitium and vascular underfilling; secondary kidney retention of sodium and water augments edema formation.
