Editing Decompression sickness (section)

=== Pathophysiology ===
The primary provoking agent in decompression sickness is bubble formation from excess dissolved gases. Various hypotheses have been put forward for the nucleation and growth of bubbles in tissues, and for the level of supersaturation which will support bubble growth. The earliest bubble formation detected is subclinical intravascular bubbles detectable by doppler ultrasound in the venous systemic circulation. The presence of these "silent" bubbles is no guarantee that they will persist and grow to be symptomatic.{{sfn|Calder 1986 |pp=241-245 }}

Vascular bubbles formed in the systemic capillaries may be trapped in the lung capillaries, temporarily blocking them. If this is severe, the symptom called "chokes" may occur.{{r|Vann 1989}} If the diver has a [[patent foramen ovale]] (or a [[shunt (medical)|shunt]] in the pulmonary circulation), bubbles may pass through it and bypass the pulmonary circulation to enter the arterial blood. If these bubbles are not absorbed in the arterial plasma and lodge in systemic capillaries they will block the flow of oxygenated blood to the tissues supplied by those capillaries, and those tissues will be starved of oxygen. Moon and Kisslo (1988) concluded that "the evidence suggests that the risk of serious neurological DCI or early onset DCI is increased in divers with a resting right–to-left shunt through a PFO. There is, at present, no evidence that PFO is related to mild or late onset bends.{{r|Moon1998}} Bubbles form within other tissues as well as the blood vessels.{{r|Vann 1989}} Inert gas can diffuse into bubble nuclei between tissues. In this case, the bubbles can distort and permanently damage the tissue.{{r|Spira 1999}} As they grow, the bubbles may also compress nerves, causing pain.{{r|Stephenson |Medscape}} [[Extravascular]] or autochthonous{{ref label|a|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.{{r|Vann 1989 |Stephenson |Kitano}}

Bubble size and growth may be affected by several factors – gas exchange with adjacent tissues, the presence of [[surfactants]], coalescence and disintegration by collision.{{sfn|Calder 1986 |pp=241–245 }} Vascular bubbles may cause direct blockage, aggregate platelets and red blood cells, and trigger the coagulation process, causing local and downstream clotting.{{r|Spira 1999}}

Arteries may be blocked by intravascular fat aggregation. [[Platelet]]s accumulate in the vicinity of bubbles. [[Endothelium|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.{{sfn|Calder 1986 |pp=241–245 }} 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.{{sfn|Calder 1986 |pp=241–245 }}

The physiological effects of a reduction in environmental pressure depend on the rate of bubble growth, the site, and surface activity. A sudden release of sufficient pressure in saturated tissue results in a complete disruption of cellular organelles, while a more gradual reduction in pressure may allow accumulation of a smaller number of larger bubbles, some of which may not produce clinical signs, but still cause physiological effects typical of a blood/gas interface and mechanical effects. Gas is dissolved in all tissues, but decompression sickness is only clinically recognised in the central nervous system, bone, ears, teeth, skin and lungs.{{sfn|Calder 1986 |pp=246–254 }}

Necrosis has frequently been reported in the lower cervical, thoracic, and upper lumbar regions of the spinal cord. 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.{{sfn|Calder 1986 |pp=246–254 }} 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. The lesions are generally discrete. Oedema usually extends to the adjacent grey matter. [[Thrombus|Microthrombi]] are found in the blood vessels associated with the infarcts.{{sfn|Calder 1986 |pp=246–254 }}

Following the acute changes there is an invasion of lipid [[phagocytes]] and degeneration of adjacent neural fibres with vascular [[hyperplasia]] at the edges of the infarcts. The lipid phagocytes are later replaced by a cellular reaction of [[astrocytes]]. Vessels in surrounding areas remain patent but are [[collagen]]ised.{{sfn|Calder 1986 |pp=246–254 }} Distribution of spinal cord lesions may be related to vascular supply. There is still uncertainty regarding the [[aetiology]] of decompression sickness damage to the spinal cord.{{sfn|Calder 1986 |pp=246–254 }}

[[Dysbaric osteonecrosis]] lesions are typically bilateral and usually occur at both ends of the [[femur]] and at the proximal end of the [[humerus]]. Symptoms are usually only present when a joint surface is involved, which typically does not occur until a long time after the causative exposure to a hyperbaric environment. The initial damage is attributed to the formation of bubbles, and one episode can be sufficient, however incidence is sporadic and generally associated with relatively long periods of hyperbaric exposure and aetiology is uncertain. Early identification of lesions by [[radiography]] is not possible, but over time areas of radiographic opacity develop in association with the damaged bone.{{sfn|Calder 1986 |pp=254–258 }}