Decompression sickness (decompression illness, caisson disease, the bends) is a disorder in which nitrogen dissolved in the blood and tissues by high pressure forms bubbles as pressure decreases.
Air is composed mainly of nitrogen and oxygen. Because air under high pressure is compressed, each breath taken at depth contains many more molecules than a breath taken at the surface. Because oxygen is used continuously by the body, the extra oxygen molecules breathed under high pressure usually do not accumulate. However, the extra nitrogen molecules do accumulate in the blood and tissues. As outside pressure decreases during ascent from a dive or when leaving a caisson, the accumulated nitrogen that cannot be exhaled immediately forms bubbles in the blood and tissues. These bubbles may expand and injure tissue, or they may block blood vessels in many organs—either directly or by triggering small blood clots. This blood vessel blockage causes pain and various other symptoms (for example, sometimes similar to those of a stroke, such as sudden weakness on one side of the body, difficulty speaking, dizziness, or even flu-like symptoms). Nitrogen bubbles also cause inflammation, causing swelling and pain in muscles, joints, and tendons.
The risk of developing decompression sickness increases with many factors, such as the following:
Because excess nitrogen remains dissolved in the body tissues for at least 12 hours after each dive, repeated dives within 1 day are more likely to cause decompression sickness than a single dive. Flying immediately after diving (such as at the end of a vacation) exposes people to an even lower atmospheric pressure, making decompression sickness slightly more likely.
Nitrogen bubbles may form in small blood vessels or in the tissues themselves. Tissues with a high fat content, such as those in the brain and spinal cord, are particularly likely to be affected, because nitrogen dissolves very readily in fats.
Decompression sickness may affect a variety of organs and can range from mild to severe. Type I decompression sickness tends to be mild and affects primarily the joints, skin, and lymphatic vessels. Type II, which may be life-threatening, often affects vital organ systems, including the brain and spinal cord, the respiratory system, and the circulatory system.
Symptoms of decompression sickness usually develop more slowly than do those of air embolism and pulmonary barotrauma. Only half of the people with decompression sickness have symptoms within 1 hour of surfacing, but 90% have symptoms by 6 hours. Symptoms commonly begin gradually and take some time to reach their maximum effect. The first symptoms may be fatigue, loss of appetite, headache, and a vague feeling of illness.
Type I (less severe):
The less severe type (or musculoskeletal form) of decompression sickness, often called the bends, typically produces pain. The pain usually occurs in the joints of the arms or legs, back, or muscles. Sometimes the location is hard to pinpoint. The pain may be mild or intermittent at first but may steadily grow stronger and become severe. The pain may be sharp or may be described as “deep” or “like something boring into bone.” It is worse when moving. Less common symptoms include itching, skin mottling, swollen lymph nodes, rash, and extreme fatigue. These symptoms do not threaten life but may precede more dangerous problems.
Type II (more severe):
The more severe type of decompression sickness most commonly results in neurologic symptoms, which range from mild numbness to paralysis and death. The spinal cord is especially vulnerable. When the spinal cord is affected, symptoms can include numbness, tingling, weakness, or a combination in the arms, legs, or both. Mild weakness or tingling may progress over hours to irreversible paralysis. Inability to urinate or inability to control urination or defecation may also occur. Pain in the abdomen and back also is common. Symptoms of brain involvement, most of which are similar to those of air embolism, include headache, confusion, trouble speaking, and double vision. Loss of consciousness is rare.
The nerves of the inner ear may be affected, causing severe vertigo, ringing in the ears, and hearing loss. Gas bubbles that travel through the veins to the lungs produce cough, chest pain, and progressively worsening difficulty breathing (the chokes). Severe cases, which are rare, may result in shock and death.
Late effects of decompression sickness include the destruction of bone tissue (dysbaric osteonecrosis, avascular bone necrosis), especially in the shoulder and hip, which produces persistent pain and severe disability. These injuries do not occur among recreational divers but, rather, among people who work in a compressed-air environment and divers who work in underwater habitats. These workers are exposed to high pressure for prolonged periods and may have an undetected case of the bends. Technical divers, who dive to greater depths than recreational divers, may be at higher risk than recreational divers. Bone and joint injuries may gradually progress over months or years to severe, disabling arthritis. By the time severe joint damage has occurred, the only treatment may be joint replacement.
Permanent neurologic problems, such as partial paralysis, usually result from delayed or inadequate treatment of spinal cord symptoms. However, sometimes the damage is too severe to correct, even with appropriate treatment. Repeated treatments with oxygen in a high-pressure chamber seem to help some people recover from spinal cord damage.
Doctors recognize decompression sickness by the nature of the symptoms and their onset in relation to diving. Tests such as computed tomography (CT) or magnetic resonance imaging (MRI) sometimes show brain or spinal cord abnormalities but are not reliable. However, recompression therapy is begun before the results of a CT or MRI scan are available, except in cases in which the diagnosis is uncertain or the diver's condition is stable. X-rays are needed to diagnose dysbaric osteonecrosis.
Divers can usually prevent decompression sickness by restricting the total amount of gas the body absorbs. The amount can be restricted by limiting the depth and duration of dives to a range that does not need decompression stops during ascent (called no-stop limits by divers) or by ascending with decompression stops as specified in authoritative guidelines, such as the decompression table in the United States Navy Diving Manual. The table provides a schedule for ascent that usually allows excess nitrogen to escape without causing harm. Many divers wear a portable dive computer that continually tracks the diver's depth and time at depth. The computer calculates the decompression schedule for a safe return to the surface and indicates when decompression stops are needed.
In addition to following a table or computer guidelines for ascent, many divers make a safety stop of a few minutes at about 15 feet (4.5 meters) below the surface.
Following these procedures, however, does not eliminate the risk of decompression sickness. A small number of cases of decompression sickness develop after no-stop dives, and the incidence of decompression sickness has not declined despite the widespread use of dive computers. The inability to eliminate decompression sickness may be because the published tables and computer programs do not completely account for the variation in risk factors among different divers or because some people fail to obey the recommendations of the tables or computer.
Other precautions also are necessary:
The Divers Alert Network (919-684-8111; www.diversalertnetwork.org) provides 24-hour consultation for diving-related problems.
About 80% of people recover completely.
Divers having only itching, skin mottling, and fatigue usually do not need to undergo recompression, but they should be kept under observation, because more serious problems may develop. Breathing 100% oxygen from a close-fitting face mask may provide relief.
Any other symptoms of decompression sickness indicate the need for treatment in a high-pressure (recompression or hyperbaric oxygen) chamber, because recompression restores normal blood flow and oxygen to affected tissues. After recompression, pressure is reduced gradually, with designated pauses, allowing time for excess gases to leave the body harmlessly. Because symptoms may reappear or worsen over the first 24 hours, even people with only mild or transient pain or neurologic symptoms are treated.
Recompression therapy is beneficial for up to 48 hours after diving and should be given even if reaching the nearest chamber requires significant travel. While awaiting transport and during transport, oxygen is administered with a close-fitting face mask, and fluids are given by mouth or intravenously. Long delays in treatment increase the risk of permanent injury.
Last full review/revision May 2013 by Alfred A. Bove, MD, PhD