Depressurisation causes inert gases, which were dissolved under higher pressure, to come out of physical solution and form gas bubbles within the body.
The most severe types of DCS interrupt — and ultimately damage — spinal cord function, leading to paralysis, sensory dysfunction, or death.
Bubble size and growth may be affected by several factors - gas exchange with adjacent tissues, the presence of surfactants, coalescence and disintegration by collision.[62]
Vascular bubbles may cause direct blockage, aggregate platelets and red blood cells, and trigger the coagulation process, causing local and downstream clotting.[65]
Extravascular or autochthonous[a] bubbles usually form in slow tissues such as joints, tendons and muscle sheaths. Direct expansion causes tissue damage, with the release of histamines and their associated affects. Biochemical damage may be as important as, or more important than mechanical effects.[63][66][68]
Arteries may be blocked by intravascular fat aggregation. Platelets accumulate in the vicinity of bubbles. Endothelial damage may be a mechanical effect of bubble pressure on the vessel walls, a toxic effect of stabilised platelet aggregates and possibly toxic effects due to the association of lipids with the air bubbles.[62]
Protein molecules may be denatured by reorientation of the secondary and tertiary structure when non-polar groups protrude into the bubble gas and hydrophilic groups remain in the surrounding blood, which may generate a cascade of pathophysiological events with consequent production of clinical signs of decompression sickness.[62]
Microthrombi are found in the blood vessels associated with the infarcts.[69]
A catastrophic pressure reduction from saturation produces explosive mechanical disruption of cells by local effervescence, while a more gradual pressure loss tends to produce discrete bubbles accumulated in the white matter, surrounded by a protein layer.[69]
Typical acute spinal decompression injury occurs in the columns of white matter. Infarcts are characterised by a region of oedema, haemorrhage and early myelin degeneration, and are typically centred on small blood vessels.
Dysbaric osteonecrosis lesions are typically bilateral and usually occur at both ends of the femur and at the proximal end of the humerus
https://en.wikipedia.org/wiki/Decompression_sickness
Dysbaric osteonecrosis or DON is a form of avascular necrosis where there is death of a portion of the bone that is thought to be caused by nitrogen embolism(blockage of the blood vessels by a bubble of nitrogen coming out of solution) in divers.[1] Although the definitive pathologic process is poorly understood, there are several hypotheses:
- Intra- or extravascular nitrogen in bones, "nitrogen embolism".[citation needed]
- Osmotic gas effects due to intramedullary pressure effects.[citation needed]
- fat embolism[citation needed]
- hemoconcentration and increased coagulability.[citation needed]
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