M04.03.14 Peripheral Edema

Peripheral edema occurs due to significant alterations in the Starling forces, leading to an imbalance that favors filtration over reabsorption. These alterations result in fluid accumulation in the interstitial spaces, often due to increased capillary permeability or impaired lymphatic drainage.

Key Mechanisms of Peripheral Edema

Peripheral edema can be triggered by a variety of factors that disrupt the balance of fluid exchange across the capillaries. Below are the primary mechanisms:

1. Increased Capillary Hydrostatic Pressure (PC)

This pressure forces more fluid out of the capillaries and into the interstitial space. Key causes include:

• Increased blood flow: Seen in cases of vasodilation in a specific vascular bed.
• Elevated venous pressure: This can occur due to venous obstruction or heart failure, where blood backs up, raising pressure in the capillaries.
• Elevated blood volume: Usually caused by sodium retention, as seen in heart failure, where increased sodium levels cause fluid retention and expanded blood volume.

2. Increased Interstitial Oncotic Pressure (πIF)

This refers to an increase in the osmotic pull exerted by solutes in the interstitial fluid, drawing more fluid out of the capillaries. Causes include:

• Thyroid dysfunction: This leads to the accumulation of mucopolysaccharides in the interstitial space, acting as osmotic agents.
• Lymphedema: This results from lymphatic dysfunction and causes fluid retention, leading to non-pitting edema.

3. Decreased Vascular Oncotic Pressure (πC)

The oncotic pressure in the blood vessels, primarily driven by proteins like albumin, helps retain fluid within the vascular compartment. Causes of decreased vascular oncotic pressure include:

• Liver failure: This leads to decreased production of plasma proteins such as albumin.
• Nephrotic syndrome: Excessive loss of proteins through the urine reduces oncotic pressure within the capillaries.

4. Increased Capillary Permeability (k)

An increase in capillary permeability allows more fluid and proteins to leak into the interstitial space, contributing to edema. This can be caused by:

• Inflammatory agents: Tumor necrosis factor-alpha (TNF-α), bradykinin, histamine, and other cytokines can increase capillary permeability, especially during burn trauma or severe inflammation.

5. Lymphatic Obstruction/Removal (Lymphedema)

The lymphatic system is responsible for clearing proteins and excess fluid from the interstitial space. When obstructed or removed, as in the case of:

• Filarial infections (e.g., Wuchereria bancrofti, causing elephantiasis),
• Bacterial lymphangitis (e.g., due to streptococci),
• Trauma, surgery, or tumors,

the inability to clear proteins leads to fluid accumulation and non-pitting edema due to increased interstitial oncotic pressure (πIF).

Summary of Mechanisms

Points to Remember

• Starling forces govern fluid exchange across capillaries and are critical in maintaining fluid balance.
• Peripheral edema occurs when filtration exceeds reabsorption due to changes in hydrostatic and oncotic pressures.
• Non-pitting edema is often seen in lymphedema, where fluid and protein accumulate in the interstitial space.
• Causes such as heart failure, liver failure, and inflammation are common contributors to different types of edema.

Bibliography

• Hall, J. E., & Guyton, A. C. (2020). Textbook of Medical Physiology. Elsevier.
• Levick, J. R., & Michel, C. C. (2010). Microvascular fluid exchange and the revised Starling principle. Cardiovascular Research, 87(2), 198-210.
• Rockson, S. G. (2001). Lymphedema. American Journal of Medicine, 110(4), 288-295.