Physiology and presentation of decompression sickness

Scuba divers need an inert gas (nitrogen) as a major component of the compressed air mix to avoid oxygen toxicity at depth. The physiology of decompression sickness is dependent on the rate at which nitrogen comes out of solution in the blood and tissues during ascent.

On descent, the partial pressure of nitrogen increases and the inert gas moves rapidly across the alveolar-capillary membrane into the arterial blood. On ascent, sufficient time is needed to allow this inert gas to clear via the lungs. If an ascent is too rapid, nitrogen is forced out of solution, forming bubbles that can travel into tissues and the venous circulation, causing decompression sickness. Decompression stops are good diving practice to facilitate nitrogen clearance. Decompression stops are not always mandated for recreational diving, and decompression sickness can still occur despite their use.

Gas bubbles can cause direct mechanical effects (by blocking vessels or damaging tissue) or activate inflammatory pathways (causing secondary adverse effects). Symptoms are determined by the volume and location of any gas bubbles that form. Bubbles arising in venous blood do not cause problems unless a person has a patent foramen ovale, atrial septal defect or pulmonary arteriovenous fistula, allowing entry into the arterial circulation.

Divers can develop decompression sickness after ascending from very short dives, in deep or shallow water, even when adhering to protocols. Decompression sickness should be strongly suspected in any diver presenting with:

• musculoskeletal complaints such as joint pain or stiffness (‘the bends’)
• profound fatigue
• skin complaints such as itch or rash
• any neurological impairment after diving
• chest pain, shortness of breath, cough.

While onset of effects is usually within an hour of surfacing, presentation for medical assistance may be delayed if the diver thinks they have mild symptoms. It is uncommon to develop new symptoms after 12 hours.

Decompression sickness is a diagnosis based on a detailed history and clinical examination. Specific investigations are not indicated unless there are concerns about concomitant barotrauma. Any neurologic symptoms after a dive are abnormal and should be attributed to decompression sickness until proven otherwise. The neurological manifestations of decompression sickness can be clinically indistinguishable from those of arterial gas embolism. The treatment of any form of decompression sickness is identical to that of arterial gas embolism—urgent referral for hyperbaric oxygen therapy.