Learning Objective: Understand the major Starling force abnormalities and lymphatic factors that contribute to peripheral edema, including how changes in hydrostatic pressure, oncotic pressure, capillary permeability, and lymphatic obstruction lead to pitting or non-pitting edema.
Peripheral Edema
Significant disturbances in the Starling forces—those that shift the balance toward filtration—along with increased capillary permeability (k) or impaired lymphatic drainage, contribute to the development of edema. Key mechanisms include:
Increased capillary hydrostatic pressure (PC)
Common causes include:
- Marked increases in blood flow (e.g., vasodilation in a local vascular bed)
- Elevated venous pressure (e.g., venous obstruction or heart failure)
- Increased blood volume from sodium retention (e.g., heart failure)
Increased interstitial oncotic pressure (πIF)
Common causes include:
- Often due to thyroid dysfunction (accumulation of mucopolysaccharides)
- Can occur with lymphedema
- The rise in interstitial solutes pulls water outward → non-pitting edema
Decreased plasma oncotic pressure (πC)
Common causes include:
- Causes include liver failure (↓ albumin synthesis) and nephrotic syndrome (protein loss)
- Reduced plasma proteins decrease the reabsorptive force → edema formation
Increased capillary permeability (k)
Occurs with circulating mediators such as:
- TNF-α
- Bradykinin
- Histamine
- Cytokines from burn trauma
These factors permit excessive fluid (and sometimes protein) to escape into the interstitium.
Lymphatic obstruction/removal (lymphedema)
Causes include:
- Filariasis (e.g., Wuchereria bancrofti → elephantiasis)
- Bacterial lymphangitis (e.g., streptococci)
- Trauma
- Surgery (e.g., axillary node dissection)
- Tumors
Since lymphatics normally clear interstitial proteins, obstruction leads to protein accumulation → non-pitting edema (due to ↑ πIF).
