I think CVC cannot lead to heart failure primarily. So let's think its pathogenesis in skin now only.

I think the pathogenesis is like this

  • dilation of veins and capillaries due to impaired venous drainage
  • reduced outflow of blood from a tissue
  • passive process
  • $\to$ local increase in blood volumes
  • $\to$ local increase in venous pressure
  • pathological
  • $\to$ shortage of oxygen and built-up metabolic waste
  • $\to$ structural changes in microvasculature
  • $\to$ increased venous permeability % hallmark of acute inflammation
  • $\to$ increased size of venous caliber
  • $\to$ emigration of leucocytes
  • $\to$ accumulation at site of injury
  • activation of acute inflammation
  • $\to$ protein into extravascular space
  • $\to$ increased viscosity of blood
  • $\to$ deoxygenated blood blood stasis
  • $\to$ congested tissue
  • $\to$ leucocytes move to endothelial wall (selectins)
  • $\to$ roll
  • $\to$ adhere (integrin to stop)
  • $\to$ migrate
  • $\to$ dysky reddish-bluish skin (cyanotic)
  • $\to$ healing via fibrosis
  • $\to$ scar
  • Causes: venous thrombosis; venous compression; heart failure;

I am not sure about the role of leucocytes exactly in this process. I am not sure if they play a big role in the formation of cyanotic skin. I think the outcome is mostly because of increased vascular permeability and its deoxygenated blood in extracellular space.

What is the right pathogenesis of chronic venous congestion in skin?


Probably so simple answer is enough

  • acrocyanosis (manifestation of heart failure) which lead to distant (acro - distant) cyanosis, bluish skin.

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