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.
(See also Overview of Diving Injuries.)
Henry’s law states that the quantity of gas dissolved in a liquid is directly proportional to the partial pressure of the gas in equilibrium with the liquid. Thus, the amount of inert gases (eg, nitrogen, helium) dissolved in the blood and tissues increases at higher pressure.
During ascent, when the surrounding pressure decreases, bubbles (mainly nitrogen) 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 blood vessels
Rupturing or compressing tissue
Inducing endothelial damage and extravasation of plasma
Activating clotting and inflammatory cascades
Because nitrogen dissolves readily in fat, tissues with a high lipid content (eg, in the central nervous system) are particularly susceptible.
Risk factors for decompression sickness
Decompression sickness occurs in about 2 to 4/10,000 dives among recreational divers. The incidence is higher among commercial divers, who are exposed to deeper depths and longer dive times. Risk factors include all of the following:
Cold-temperature dives
Dehydration
Exercise after diving
Fatigue
Flying after diving
Obesity
Older age
Prolonged or deep dives
Rapid ascents
Right-to-left cardiac shunts
Because excess nitrogen remains dissolved in body tissues for at least 12 hours 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).
Classification of decompression sickness
Decompression sickness is classified as follows:
Type I: Involves joints, skin, and lymphatics and is milder and not typically life threatening
Type II: Includes neurologic or cardiorespiratory involvement, which is serious, is sometimes life threatening, and affects various organ systems
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.
The term decompression illness refers to either decompression sickness or arterial gas embolism.
General references
Vann RD, Butler FK, Mitchell SJ, et al: Decompression illness. Lancet 377(9760):153-164, 2011. doi: 10.1016/S0140-6736(10)61085-9
Mitchell SJ, Bennett MH, Moon RE: Decompression sickness and arterial gas embolism. N Engl J Med 386(13):1254-1264, 2022. doi: 10.1056/NEJMra2116554
Symptoms and Signs of Decompression Sickness
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 hour of surfacing in about 50% of patients and by 6 hours in 90%. Rarely, symptoms can manifest 24 to 48 hours after surfacing, particularly by exposure to altitude after diving (such as air travel).
Type I decompression sickness typically causes pain in the joints (most commonly elbows and shoulders) and occasionally muscles; the pain typically does not intensify during movement and is described as “deep” and “boring.” Other manifestations include lymphedema, skin mottling, itching, and rash.
Type II decompression sickness consists of 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, cough, resulting from pulmonary edema. 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 and often occurs without any previous symptoms. 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 disability due to secondary osteoarthritis.
Deep vein thrombosis and pulmonary embolism can complicate immobility due to decompression sickness.
Diagnosis of Decompression Sickness
Clinical evaluation
Diagnosis is clinical. CT and MRI may be helpful to rule out other disorders that cause similar symptoms (eg, herniated intervertebral disk, ischemic stroke, central nervous system hemorrhage). Although these studies sometimes show brain or spinal cord abnormalities due to decompression sickness, their sensitivity for decompression sickness is low, 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 ). However, immediate treatment for both is similar.
Comparison of Gas Embolism and Decompression Sickness
Feature | Gas Embolism | Decompression Sickness |
|---|---|---|
Symptoms and signs | Common: Unconsciousness, often with seizures (any diver who loses consciousness shortly after surfacing should be assumed to have arterial gas embolism and should be recompressed promptly) Less common: Milder cerebral manifestations, signs of pulmonary barotrauma (eg, mediastinal or subcutaneous emphysema, pneumothorax) | Extremely variable—the bends (pain, most often in or near a joint), neurologic manifestations of almost any type or degree, and the chokes (respiratory distress followed by circulatory collapse—an extreme emergency), occurring alone or with other symptoms |
Onset | Sudden, usually during or within a few minutes after surfacing | Usual: Gradual or sudden, with symptoms developing ≥ 1 hour after surfacing in about 50%; onset up to 24 hours after dives* of > 10 m (> 33 ft) or hyperbaric exposures of > 2 ATA Rare: Symptoms developing > 24 hours after surfacing is rare although altitude exposure (eg, commercial aircraft flight) can cause delayed onset |
Proximate cause | Usual: Breath holding or airway obstruction during ascent (even from a meter [a few feet] of depth, particularly when ascent is rapid); air trapped in the lungs expands during ascent and causes lung tissue injury Occasional: Severe decompression sickness resulting in arterial bubbles or intrapulmonary gas trapping due to preexisting lung disease (eg, bullae, interstitial lung disease) | Usual: Diving or hyperbaric exposure, especially beyond no-stop limits Occasional: Diving or hyperbaric exposure to shallow depths (12 m [40 ft] or shallower); low-pressure exposure (eg, flying after diving) |
Mechanism | Usual: Overinflation of lungs causing entry of free gas into pulmonary vessels followed by embolization of cerebral vessels Occasional: Coronary, renal, or cutaneous circulatory obstruction by free gas from any source | Formation of bubbles from excess dissolved gas in blood or tissue when external pressure decreases |
Emergency treatment | Essential emergency care as needed (eg, airway patency, hemostasis, CPR or mechanical ventilation) Prompt transport to nearest recompression chamber Horizontal position if needed to maintain blood pressure Unconscious patients with impaired airway reflexes should be kept in the lateral decubitus position to help prevent aspiration, if tracheal intubation is not feasible 100% oxygen by close-fitting mask Fluids orally if patient is conscious; otherwise, IV Arterial gas embolism after only a short, shallow dive may not require aggressive fluid administration | Essential emergency care as needed (eg, airway patency, CPR or mechanical ventilation) Prompt transport to nearest recompression chamber Horizontal position if needed to maintain blood pressure Unconscious patients with impaired airway reflexes should be kept in the lateral decubitus position to help prevent aspiration, if tracheal intubation is not feasible 100% oxygen by close-fitting mask Fluids orally if patient is conscious; otherwise, IV |
* Repeat dives are frequently involved. | ||
ATA = atmospheres absolute; CPR = cardiopulmonary resuscitation. | ||
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.
Pearls & Pitfalls
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Treatment of Decompression Sickness
100% oxygen
Recompression therapy
Fluid therapy to maintain intravascular volume
The majority of patients recover completely.
Initially, high-flow 100% oxygen enhances nitrogen washout by widening the nitrogen pressure gradient between the lungs and the circulation, thus accelerating reabsorption of nitrogen-containing embolic bubbles.
To restore lost intravascular volume, oral resuscitation fluid (or plain water) is indicated for alert patients with mild manifestations. Isotonic, glucose-free IV fluids are indicated for those with serious manifestations.
Recompression therapy is indicated for all patients except perhaps those whose symptoms are limited to itching, skin mottling, and fatigue, which may be treatable with oxygen alone; patients should be observed for deterioration (1). Patients with more severe symptoms 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]) should ideally be maintained and oxygen given continuously. Commercial aircraft, although pressurized, typically have a cabin pressure up to an equivalent of 2438 m (8000 ft) at normal cruise altitude, which may exacerbate symptoms. Flying in commercial aircraft shortly after a dive can precipitate symptoms. The risk of altitude exposure in patients with decompression illness should be balanced against the risk of deterioration if not evacuated for definitive treatment.
When symptoms are mild (eg, normal neurologic examination and stable for 24 hours), delayed recompression or evacuation by commercial airliner is unlikely to worsen long-term outcome.
Because decompression sickness or arterial gas embolism can be complicated by deep vein thrombosis and pulmonary thromboembolism, periodic ultrasonography of the leg veins should be considered.
Treatment references
1. Moon RE, Mitchell S: Hyperbaric treatment for decompression sickness: Current recommendations. Undersea Hyperb Med, 46(5):685-693, 2019. PMID: 31683368.
2. Mitchell SJ, Bennett MH, Moon RE: Decompression sickness and arterial gas embolism. N Engl J Med 386(13):1254-1264, 2022. doi: 10.1056/NEJMra2116554
Prevention of Decompression Sickness
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 and Arterial Gas Embolism in the U.S. 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, cases can occur after appropriately identified no-stop dives, and the incidence of decompression sickness has not decreased despite widespread use of dive computers (although fewer serious cases occur).
Dives < 24 hours apart (repetitive dives) and dives performed at altitude require special techniques to determine proper decompression procedures.
Key Points
Symptoms of decompression sickness develop within 1 hour of surfacing in 50% of affected patients and within 6 hours in 90%.
If the disorder is suspected, start high-flow 100% oxygen 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.
More Information
The following English-language resources may be useful. Please note that THE MANUAL is not responsible for the content of these resources.
Divers Alert Network: 24-hour emergency hotline, 919-684-9111
Duke Dive Medicine: Physician-to-physician consultation, 919-684-8111
Undersea and Hyperbaric Medical Society: Scientific and medical information pertaining to undersea and hyperbaric medicine through its bimonthly, peer-reviewed journal, Undersea and Hyperbaric Medicine, and other resources
U.S. Navy Diving Manual: Detailed reference guide published by the US Navy detailing diver training and diving operations
