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?


1 Answer 1


Probably so simple answer is enough

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

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