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(Caisson Disease; The Bends)
Decompression sickness occurs when rapid pressure reduction (eg, during ascent from a dive, exit from a caisson or hyperbaric chamber, or ascent to altitude) causes gas previously dissolved in blood or tissues to form bubbles in blood vessels. Symptoms typically include pain, neurologic symptoms, or both. Severe cases can be fatal. Diagnosis is clinical. Definitive treatment is recompression therapy. Proper diving techniques are essential for prevention.
Henry’s law states that the solubility of a gas in a liquid is directly proportional to the pressure exerted on the gas and liquid. Thus, the amount of inert gases (eg, N2, helium) dissolved in the blood and tissues increases at higher pressure.
During ascent, when the surrounding pressure decreases, bubbles (mainly N2) may form. The liberated gas bubbles can arise in any tissue and cause local symptoms, or they can travel via the blood to distant organs ( arterial gas embolism). Bubbles cause symptoms by blocking vessels, rupturing or compressing tissue, or activating clotting and inflammatory cascades. Because N2 dissolves readily in fat, tissues with a high lipid content (eg, in the CNS) are particularly susceptible.
Decompression sickness occurs in about 2 to 4/10,000 dives among recreational divers. The incidence is higher among commercial divers, who often have minor musculoskeletal injuries. Risk factors include all of the following:
Because excess N2 remains dissolved in body tissues for at least 12 h after each dive, repeated dives within 1 day are more likely to cause decompression sickness. Decompression sickness can also develop if pressure decreases below atmospheric pressure (eg, by exposure to altitude).
Generally, there are 2 types of decompression sickness:
The spinal cord is especially vulnerable; other vulnerable areas include the brain, respiratory system (eg, pulmonary emboli), and circulatory system (eg, heart failure, cardiogenic shock).
The bends refers to local joint or muscle pain due to decompression sickness but is often used as a synonym for any component of the disorder.
Severe symptoms may manifest within minutes of surfacing, but in most patients, symptoms begin gradually, sometimes with a prodrome of malaise, fatigue, anorexia, and headache. Symptoms occur within 1 h of surfacing in about 50% of patients and by 6 h in 90%. Rarely, symptoms can manifest 24 to 48 h after surfacing, particularly by exposure to altitude after diving (such as air travel).
Type I decompression sickness typically causes progressively worsening pain in the joints (typically elbows and shoulders), back, and muscles; the pain intensifies during movement and is described as “deep” and “boring.” Other manifestations include lymphadenopathy, skin mottling, itching, and rash.
Type II decompression sickness tends to cause neurologic and sometimes respiratory symptoms. It typically manifests with paresis, numbness and tingling, difficulty urinating, and loss of bowel or bladder control. Headache and fatigue may be present but are nonspecific. Dizziness, tinnitus, and hearing loss may result if the inner ear is affected. Severe symptoms include seizures, slurred speech, vision loss, confusion, and coma. Death can occur.
The chokes (respiratory decompression sickness) is a rare but grave manifestation; symptoms include shortness of breath, chest pain, and cough. Massive bubble embolization of the pulmonary vascular tree can result in rapid circulatory collapse and death.
Dysbaric osteonecrosis is a late manifestation of decompression sickness. It is an insidious form of osteonecrosis caused by prolonged or closely repeated exposures to increased pressure (typically in people working in compressed air and in deep commercial rather than recreational divers). Deterioration of shoulder and hip articular surfaces can cause chronic pain and severe disability.
Diagnosis is clinical. CT and MRI may be helpful to rule out other disorders that cause similar symptoms (eg, herniated intervertebral disk, ischemic stroke, CNS hemorrhage). Although these studies may show brain or spinal cord abnormalities, they are not sensitive for decompression sickness, and treatment should usually begin based on clinical suspicion.
Arterial gas embolism can have similar manifestations (for a comparison of features, see Table: Comparison of Gas Embolism and Decompression Sickness).
For dysbaric osteonecrosis, skeletal x-rays may show joint degeneration, which cannot be distinguished from that caused by other joint disorders; MRI is usually diagnostic.
About 80% of patients recover completely.
Initially, high-flow 100% O2 enhances N2 washout by widening the N2 pressure gradient between the lungs and the circulation, thus accelerating reabsorption of embolic bubbles.
Recompression therapy is indicated for all patients except perhaps those whose symptoms are limited to itching, skin mottling, and fatigue; they should be observed for deterioration. Other patients are transported to a suitable recompression facility. Because time to treatment and severity of the injury are important determinants of outcome, transport should not be delayed for performance of nonessential procedures.
If air evacuation is required, an aircraft capable of 1 atmosphere internal pressure is preferred. In unpressurized aircraft, low altitude (< 609 m [< 2000 ft]) must be maintained. Commercial aircraft, although pressurized, typically have a cabin pressure equivalent to 2438 m (8000 ft) at normal cruise altitude, which may exacerbate symptoms. Flying in commercial aircraft shortly after a dive can precipitate symptoms.
Significant bubble formation can usually be avoided by limiting the depth and duration of dives to a range that does not need decompression stops during ascent (called no-stop limits) or by ascending with decompression stops as specified in published guidelines (eg, the decompression table in the chapter Diagnosis and Treatment of Decompression Sickness in the US Navy Diving Manual ). Many divers wear a portable dive computer that continually tracks depth and time at depth and calculates a decompression schedule.
In addition to following published and computer-generated guidelines, many divers make a safety stop for a few minutes at about 4.6 m (15 ft) below the surface. However, a few cases develop after appropriately identified no-stop dives, and the incidence of decompression sickness has not decreased despite widespread use of dive computers. The reason may be that published tables and computer programs do not completely account for the variation in risk factors among divers or that people do not follow the recommendations precisely.
Dives < 24 h apart (repetitive dives) require special techniques to determine proper decompression procedures.
Symptoms of decompression sickness develop within 1 h of surfacing in 50% of affected patients and within 6 h in 90%.
Severe decompression sickness with brain dysfunction within minutes of surfacing may be difficult to differentiate from arterial gas embolism.
If the disorder is suspected, start high-flow 100% O2 and arrange the most expeditious transport to a recompression facility possible, using ground transportation or an aircraft capable of 1 atmosphere of internal pressure.
Counsel divers to follow established recommendations (eg, diving depth and duration, use of decompression stops during ascent) that decrease the risk of decompression sickness.
Divers Alert Network : 24-hour emergency hotline, 919-684-9111
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