Bubble formation from dissolved nitrogen in tissues is plausible wherever the supersaturation conditions are favourable. However, this is the least understood and documented of the processes likely to contribute to DCS mainly because, unlike bubbles moving in blood, tiny bubbles in tissue are difficult to detect with current technology, and studying small pathological bubbles in tissue post mortem is notoriously difficult.
The spinal cord is the most scrutinized organ in this regard. The 1990s saw a number of studies published that demonstrated ‘non-staining space-occupying lesions’ 20 to 200 micrometres in diameter and presumed to be bubbles in the spinal cord white matter after provocative decompressions. These experiments determined that the supersaturation threshold was moderately high for formation of these bubbles and that significant bubbling in the spinal cord white matter was unlikely unless dives were deeper than 25 metres. They also determined that tissue bubbles tend to form in the spinal cord early, because as supersaturation declines quickly after surfacing the probability of bubble formation also rapidly declines.
The brain tissue is not considered a likely site for bubble formation because of its luxurious perfusion, which prevents significant or prolonged supersaturation after most plausible decompressions. However, nitrogen is eliminated more slowly from the inner ear than the brain, and there is some experimental evidence for bubble formation in inner ear tissue itself. The inner ear is also uniquely vulnerable to enhancement of local tissue supersaturation by a process frequently referred to as ‘isobaric counterdiffusion’ (IBCD). This can arise during decompression from deep dives in which the diver makes a switch from a breathing mix containing helium to one containing nitrogen (see Chapter 62). Such switches are undertaken in the belief that they accelerate decompression because helium in the tissues will diffuse into blood faster than the nitrogen in the blood will diffuse into the tissue. The inner ear has a unique and relevant anatomy. There are relatively large unperfused reservoirs of helium (in the perilymph and endolymph) that can eliminate accumulated helium only via the vascularized labyrinthine tissue. This maintains an elevated partial pressure of helium in the vascular labyrinth after the switch to a nitrogen-based mix, while at the same time this tissue is also exposed to high pressures of nitrogen diffusing inward from the blood stream. This ‘counterdiffusion’ process may transiently enhance any pre-existing supersaturation of helium and result in bubble formation.
In addition to clinically relevant and largely proven tissue bubble formation in the spinal cord and inner ear, there is strong circumstantial evidence that tissue bubble formation is the cause of musculoskeletal pain in DCS. Specifically, the lack of any association between the presence of PFO and musculoskeletal pain in DCS suggests that in situ bubble formation is the most likely cause, rather than bubbles arriving in the arterial blood. The exact location of tissue bubbles responsible for musculoskeletal pain is unknown, but there are multiple possibilities including tendons, ligaments, periosteum and marrow. Similar reasoning has led to the hypothesis that bubbles may form in peripheral nerve tissues. Patchy paraesthesiae in a non-dermatomal distribution are common symptoms that have not been linked to the presence of a right-to-left shunt, and it follows that tissue bubble formation is the likely cause. It is plausible that bubbles could form in the myelin of a peripheral nerve, or elsewhere within the perineurium, and cause neurapraxia through a mass effect. However, this mechanism is not substantively proven.
Finally, one presumed location for bubble formation most appropriately categorized as ‘tissue’ is the lymphatic system. The infrequent occurrence of discrete regional areas of oedematous soft tissue swelling, often accompanied by other symptoms of DCS, has led to the assumption that bubbles may form in lymphatic drainage channels and cause stasis.