Decompression sickness happens when inert gas dissolved in the tissues forms bubbles as the ambient pressure drops too fast. Symptoms range from joint pain to serious neurological problems. The standard treatment combines 100% oxygen and recompression in a hyperbaric chamber, and the sooner it starts, the better the outlook.
Decompression sickness is the accident that defines the limits of commercial diving. It is not a distant risk or a rarity: it is the reason tables, ascent times, chambers on board and much of the procedure a diver repeats every day without thinking about it all exist. Understanding it properly is not theory, it is part of the trade.
What happens inside the body
When a person breathes gas under pressure, the tissues absorb inert gas (nitrogen in air and nitrox, helium in deep mixes) until they get close to equilibrium with the ambient pressure. That gas is dissolved, it does not form bubbles, and it causes no problem as long as the pressure is held.
The problem comes on the way up. If the ambient pressure falls faster than the body can clear that gas through the lungs, the dissolved gas comes out of solution and forms bubbles. It is the same phenomenon you see opening a bottle of fizzy water, with the difference that here the bubbles form inside joints, muscles, the spinal cord, the inner ear or the pulmonary circulation.
The bubbles cause harm in two ways. Mechanically: they take up space, compress tissue and block vessels. And they trigger an inflammatory response and disrupt clotting, which explains why some cases worsen over hours, and why treatment is not just about "crushing the bubble".
It is worth distinguishing two accidents that are often lumped together under the term decompression sickness for convenience. One is decompression sickness proper, from dissolved gas. The other is arterial gas embolism, which happens when a pulmonary barotrauma pushes gas directly into the arterial circulation, typically from ascending with the airway closed. The symptoms overlap, the initial treatment is similar, but the mechanism is different.
How it shows itself
The classic presentation splits into two broad groups, and that division is still useful even though it is imperfect.
Type I cases
These are the so-called musculoskeletal "bends": deep, dull, poorly localised pain, often in the shoulder, elbow, knee or hip, that does not ease with movement. Skin manifestations, such as mottling, and lymphatic involvement with localised swelling are also included here.
Being labelled type I does not mean they are trivial. Joint pain after a dive with decompression is reason enough to put the diver on oxygen and activate the protocol.
Type II cases
These are the serious ones. They include neurological involvement (tingling, loss of strength, altered sensation, difficulty walking, urinary retention, confusion), inner ear involvement with severe vertigo, nausea and hearing loss, and the cardiorespiratory form, known as chokes, with chest pain, coughing and breathing difficulty.
Spinal cord involvement is especially feared because it can leave permanent after-effects if treatment is delayed. In an offshore environment, where the diver works far from a hospital, that is exactly why vessels and sites carry a chamber and trained personnel.
What increases the risk
No single factor on its own explains an accident, but there are conditions that come up again and again in the analysis:
- Failure to follow the decompression profile: fast ascents, missed stops or loss of depth control. It is the most direct cause, and the most avoidable.
- Deep or repeated dives with little time between them, leaving a high gas load at the start of the next one.
- Intense physical exertion during the dive, and also immediately after ascending.
- Cold and dehydration, which affect tissue perfusion and gas elimination.
- Exposure to altitude shortly after diving, including the flight home, because it reduces the ambient pressure even further.
- Factores individuales, including the presence of a patent foramen ovale, which has been linked to cases with neurological symptoms from venous bubbles passing into the arterial circulation.
A good part of the commercial diving medical exists precisely to catch conditions that make this risk worse. In what the commercial diving medical certificate assesses we go into it in more detail.
What is done when it happens: the treatment
Primeros auxilios
The first measure is normobaric oxygen at the highest percentage possible, ideally 100% through a high-flow mask or closed circuit. The aim is twofold: to increase the gradient that helps clear the dissolved inert gas, and to oxygenate the tissue the bubbles are compromising. This goes together with hydration and keeping the casualty resting and warm.
The second measure is to set the transfer in motion. On a commercial diving team this is written into procedure: supervisor, life support technician, referring doctor and, if needed, evacuation. Nobody waits to see if the symptom clears on its own.
Recompression in the chamber
The definitive treatment is recompression with hyperbaric oxygen. Raising the pressure shrinks the bubbles and helps them reabsorb; breathing oxygen under pressure speeds up clearance of the inert gas and oxygenates ischaemic tissue.
The treatment tables most widely used in the professional world come from the US Navy. The usual reference for most cases is Table 6, which compresses the patient to a pressure equivalent to 18 metres of seawater and alternates periods of oxygen with air breaks to reduce the risk of oxygen toxicity, with the option of extending it depending on the clinical response. Which table is applied, and for how long, is decided by the doctor in charge, not the diving team.
The factor that weighs most on the outcome is time. Treatment started early improves the chances of full recovery; a delay of hours, especially in spinal cases, increases the likelihood of lasting after-effects.
Why saturation diving handles it differently
In surface-supplied diving, every working day ends with a decompression. Every ascent is a chance for something to go wrong, and the number of exposures builds up over a campaign.
Saturation diving flips that approach. As we explain in what a saturation diver is, once the tissues are saturated with inert gas, staying under pressure longer does not add any more dissolved gas. The divers live pressurised in the system for the whole campaign, go down to work from the bell at a pressure equivalent to the bottom depth, and return to the system without decompressing. There is only one decompression, the final one, and it is done extremely slowly and under control, with the medical team and all the resources on board.
The result is that the risk changes in nature. The dozens of daily decompressions disappear, but other scenarios of their own appear: a loss of pressure in the bell, a failure in mix control, or the need to interrupt a decompression in progress for a medical emergency. It is also why a saturation system is, in practice, a hyperbaric treatment facility: if something happens, recompression does not require moving anyone. We sum up the difference between the two worlds in saturation diving frente a surface-supplied diving.
Prevention: what actually works
Prevention in commercial diving does not depend on the diver's intuition, but on the system around him: calculated profiles that are followed, supervision from the surface, strict control of the mixes, limited bottom times, reliable communication equipment and a rehearsed emergency chain. The recognised certifications and the schools serious ones dedicate a very substantial part of their training to this, and the contracting companies audit it.
On an individual level, there is room to cut risk: turning up rested and hydrated, reporting any symptom without playing it down, respecting the intervals before flying, and not hiding your medical history at the check-up. None of that is heroic. All of it helps prevent accidents.
And there is one rule worth taking to heart before you ever set foot on a job: when in doubt, treat it. An ambiguous symptom after a dive with decompression is managed as decompression sickness until a doctor says otherwise. Waiting to be sure is exactly what makes the outcome worse.
Frequently asked questions
What exactly causes decompression sickness?
The formation of inert gas bubbles, usually nitrogen or helium, in the blood and tissues when the ambient pressure drops faster than the body can clear that gas through breathing.
How long do symptoms take to appear?
Most cases show up in the first few hours after leaving the water, often within the first hour. A case appearing many hours later is less common, but it happens, and it should not be ruled out just because of the delay.
Does 100% oxygen cure decompression sickness?
It does not replace the definitive treatment, but it is the first measure and it improves the outlook. It increases the gradient for clearing the inert gas and oxygenates the affected tissue while the transfer to a recompression chamber is arranged.
Can you dive again after having it?
It depends on the type of accident, any after-effects, and the diving doctor's judgement. In the commercial world, returning to work goes through a specific review and formal medical fitness, not the diver's own sense of having recovered.
Why does saturation diving only decompress once?
Because once the tissues are saturated with inert gas, staying under pressure longer does not add any more dissolved gas. That allows weeks of work followed by a single final decompression, controlled and slow, instead of one every working day.
Does a patent foramen ovale rule out professional diving?
Not automatically, but it is a finding the diving doctor takes into account, because it has been linked to some cases of decompression sickness with neurological symptoms. The decision is always medical and individual.
Published 23 August 2026 · By Arthur More, professional saturation diver
Photo: SFU - Communications & Marketing · CC BY via Openverse