Venous pressure ^

Capillary hydraulic pressure ^

Transudate to interstitium |


Cardiac output

Plasma osmotic pressure

Effective blood volume


AVP Renin-Angitensin-Aldosterone |

Sodium and water retention

Sodium and water retention i

Effective blood volume |

Injury, sepsis, endotoxemia

Inflammatory response vasodilatation

Capillary hydraulic pressure ^

Inflammatroymediators (IL-1, TNF, histamine)

Vascular permeability ^

Capillary hydraulic pressure ^

Figure 1 The hemodynamic (A) and inflammatory (B) events leading to edema formation. (see color insert)

failing heart. This leads to further edema formation inflicted by the transient increase in the central venous pressure. Thus, a vicious cycle is created whereby compensatory mechanisms are constantly activated in order to increase the effective arterial blood volume but ultimately fluid escapes to the interstitium, thereby lowering again the effective arterial blood volume and further increasing edema formation [6].

Increased hydraulic pressure may also be involved in the pathogenesis of local edema formation. For example, obstruction of venous return from a limb secondary to major vein thrombosis may lead to a marked increase in the local venous pressure that overcomes the colloid osmotic pressure gradient, resulting in local accumulation of fluid in the interstitial space of the affected limb.

Reduced Plasma Oncotic Pressure

This cause for edema is less common than increased hydraulic pressure, but when it is involved in the pathogen-esis of edema formation, it tends to create a severe form of generalized edema. In most instances, the critical level of plasma protein needed to maintain adequate plasma oncotic pressure is 2.5mg/dL. A decrease in the critical content of plasma proteins, such as may occur in several clinical settings including cirrhosis of the liver, nephrotic syndrome, malnutrition, and various protein-losing gastroenter-opathies, will significantly reduce the oncotic pressure responsible for reabsorption of interstitial fluids. This favors the net movement of fluids from the intravascular compart ment to the interstitial space. The reduction in the intravascular volume leads to a state of decreased effective arterial blood volume and, as in the pathogenesis described earlier for congestive heart failure, activation of multiple compensatory pathways. As such, decreased renal blood flow will decrease the glomerular filtration rate and activate the renin-angiotensin-aldosterone axis, resulting in increased reabsorption of sodium and water. However, the resultant expansion of the intravascular volume will rapidly move to the interstitium because of the low plasma osmotic pressure, resulting in the massive fluid shift. Again, this compensatory mechanism may lead to the same vicious cycle as described in the case of heart failure, whereby renal sodium and water retention are continuously activated secondary to a sustained perceived decrease in effective arterial blood volume.

Sodium Retention

The sodium body content is the main determinant of volume in the extracellular compartment. Hence, sodium retention, which is the result of an imbalance in renal tubule sodium reabsorption relative to filtered load, may result in excessive fluid accumulation in the interstitial compartment. In generalized edema, the expansion of the extracellular volume is invariably associated with renal sodium retention. Some of the causes and pathways leading to sodium retention were outlined earlier. In congestive heart failure and cirrhosis with ascites, the primary disturbance leading to sodium retention does not originate within the kidney. Instead, renal sodium retention is the response to a disturbance of the effective circulation induced by disease of the heart or liver. In the nephrotic syndrome, glomerular injury accompanied by heavy proteinuria is associated with sodium retention and leads to a profound disturbance in circulatory homeostasis. In each of these conditions, the renal effector mechanisms that normally operate to conserve sodium and protect against a sodium deficit are exaggerated and continue despite subtle or overt expansion of interstitial compartment volume.

Inadequate Lymphatic Flow

This form of edema, commonly termed lymphedema, is nearly always confined to a specific anatomic region. Under normal circumstances, excess of interstitial fluid is removed by the lymphatic system, eventually returning to the circulation through the thoracic duct. Lymphatic obstruction is commonly observed in the arms following axillary lymph node dissection or irradiation, and in the lower extremities following inguinal lymph node dissection or chronic infection with the filarial worm Wuchecheria bancrofti. This form of edema may be massive and severely impair limb function, again demonstrating the important role of the lymphatic network in minimizing edema formation.

In summary, changes in any one or more of the factors that contribute to Starling forces may result in violation of the normal body fluid partitioning and the development of edema. The magnitude of edema is therefore a reflection of the intensity of the hemodynamic derangement, and every attempt should be made to identify the cause and aim treatment strategies to counter these factors.

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Essentials of Human Physiology

Essentials of Human Physiology

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