Bubbles or microparticles: which are the main initial cause of decompression illness?

There are two leading schools of thought on the mechanism that causes decompression illness (DCI). The old school attributes DCI to decompression bubbles, while the new school, mostly led by S. Thom, attributes DCI mainly to microparticles (MP).

Microparticles were found to be elevated at high pressures before decompression and, more so, after decompression. Decompression MP activate neutrophils and platelets, enhance inflammation, stimulate proinflammatory cytokines, and proto-coagulant activity. The predominant presence of endothelial MP is obvious. It was suggested that large MP contain a gas phase of nitric oxide (NO) and its derivatives and serve as gas micronuclei for decompression bubbles. Formation of a gas phase from very soluble NO is unlikely.

Bubbling is crucial in the decompression from depth, and one cannot simply shoot up from the depth to the surface. The inconsistency between the relations of venous bubbles and DCI can be related to DCI unrelated to shunted/non-shunted venous bubbles, like distal arterial bubbles and local bubble formation. It was suggested that a detached bubble tears off the underlying endothelial cells, and when the bubble becomes lodged in the lung, it diminishes to a gas-containing microparticle enveloped by an endothelial membrane.

The main initial cause for DCI is the formation of decompression bubbles, and microparticles add to the injury but would not cause DCI without decompression bubbles.