Pathophysiology of Decompression Illness

Decompression illness (DCI) is the umbrella term used to encompass both decompression sickness (DCS) and arterial gas embolism (AGE).

Decompression Sickness

Decompression sickness is caused by nitrogen coming out of solution when a diver ascends from a dive. It is sometimes described as being caused by evolved gas. The inert gas that evolves from the tissues can then cause a mass effect and inflammatory response in that tissue. This can happen anywhere in the body but is commonly seen in the articular cartilage (joints) and nervous tissue especially the spinal cord.

The full mechanism and pathophysiology of DCS is poorly understood and still being researched. It is thought there are two main effects from evolved gas:

  1. Direct damage (PRIMARY). Direct damage to the tissue resulting from the gas bubbles is thought to be caused by artery occlusion, damage to vascular endothelium and venous outflow obstruction. The effects on the vessels results in a disturbance of vascular permeability and microvascular flow which can cause a breakdown in the blood brain barrier4
  2. Inflammatory response (SECONDARY). Gas bubbles cause secondary effects by activating the clotting cascade, platelets, complement and leucocytes resulting in an inflammatory response in the affected tissues3.

Due to these two mechanisms of tissue damage DCI can present anytime from 0-72 hours or more after a dive. The symptoms due to the direct effect of bubbles usually present quickly whereas inflammatory responses can cause a latent response. This also means that DCI can have an evolving course with inflammatory mediated symptoms worsening over time.