Decompression sickness (DCS), commonly known as “the bends,” occurs when a reduction in ambient pressure results in the formation of inert gas bubbles within tissues or the circulation. These bubbles can produce musculoskeletal pain, cutaneous manifestations, neurologic dysfunction, cardiopulmonary compromise, and, in severe cases, shock or death.
Hyperbaric Oxygen Therapy (HBOT), also referred to as recompression therapy in diving medicine, is the definitive treatment for clinically significant decompression sickness and is recognized by the Undersea & Hyperbaric Medical Society (UHMS) as an accepted indication for hyperbaric treatment.
Suspected DCS should be treated as a time-sensitive medical condition. Initial management includes high-concentration oxygen, appropriate stabilization, and prompt consultation with clinicians experienced in diving and hyperbaric medicine.
When decompression sickness is suspected, early recognition and coordination of definitive care are important.
Patients with neurologic, vestibular, cardiopulmonary, or progressive manifestations require particularly urgent evaluation.
The initial response to surface oxygen should not be used by itself to determine that hyperbaric treatment is unnecessary. Symptoms may improve or disappear during oxygen administration and later recur.
Likewise, a delay in presentation should not automatically exclude a patient from recompression. Although earlier treatment is generally preferred, patients presenting after a delay may still benefit from evaluation and HBOT.
During exposure to increased ambient pressure, such as during compressed-gas diving, inert gas—primarily nitrogen or helium depending on the breathing mixture—dissolves into the body's tissues.
During ascent and decompression, this dissolved gas must be eliminated gradually through the circulation and lungs.
When ambient pressure decreases sufficiently and tissue inert-gas tension exceeds the surrounding pressure, tissues become supersaturated. Inert gas may then come out of solution and form bubbles.
DCS can occur after:
Scuba diving
Surface-supplied or commercial diving
Saturation or technical diving
Rapid ascent from depth
Missed or inadequate decompression
Repetitive diving
Rapid ascent to altitude
Loss of aircraft cabin pressure
Hypobaric chamber exposure
Decompression from certain hyperbaric environments
Spaceflight or extravehicular activity
Although DCS is most commonly associated with compressed-gas diving, it is fundamentally a disorder caused by decompression and can therefore occur in other circumstances involving substantial reductions in ambient pressure.
The terms decompression sickness and decompression illness are sometimes used interchangeably, but they do not have exactly the same meaning.
Decompression sickness (DCS) results from inert gas coming out of solution and forming bubbles following decompression.
Arterial gas embolism (AGE) generally occurs when gas enters the arterial circulation, often following pulmonary barotrauma during ascent.
The broader term decompression illness (DCI) encompasses both DCS and arterial gas embolism because their clinical presentations can overlap and their initial emergency management and recompression treatment may be similar.
This distinction can be difficult to make immediately after a diving accident and should not delay appropriate treatment.
The effects of decompression sickness extend beyond the simple presence of gas bubbles.
Bubbles may cause direct mechanical obstruction and tissue distortion, but they can also initiate a complex secondary inflammatory and vascular response.
Potential mechanisms include:
Mechanical obstruction of blood flow
Direct tissue distortion
Endothelial dysfunction
Platelet activation
Activation of coagulation pathways
Capillary leakage
Complement activation
Leukocyte-endothelial interactions
Tissue edema
Impaired microcirculatory perfusion
Local and systemic inflammatory responses
The location and distribution of bubbles help determine the clinical manifestations.
Neurologic DCS may involve the spinal cord, brain, peripheral nerves, or vestibular system. Pulmonary involvement can produce severe cardiopulmonary manifestations, while bubbles within musculoskeletal tissues may produce characteristic joint or limb pain.
Decompression sickness has a highly variable presentation. Symptoms may begin shortly after surfacing or decompression, although onset can be delayed.
Musculoskeletal DCS may cause:
Pain may occur without swelling, tenderness, or other obvious physical findings.
Inner-ear decompression sickness may present with:
These manifestations can sometimes be difficult to distinguish from inner-ear barotrauma, making consultation with an experienced diving-medicine physician particularly important.
Severe DCS may cause:
Pulmonary decompression sickness has historically been referred to as “the chokes” and represents a potentially life-threatening presentation.
Neurologic decompression sickness may produce:
Spinal cord involvement is an especially important manifestation of severe DCS and may progress rapidly.
Skin findings may include:
A characteristic mottled or marbled appearance, sometimes referred to as cutis marmorata, can be associated with significant decompression illness and should not automatically be considered a minor manifestation.
Recompression addresses both the physical gas phase and the secondary pathophysiologic effects of decompression sickness.
Increasing ambient pressure compresses gas bubbles. Reducing bubble volume may decrease mechanical tissue distortion and vascular obstruction and improve perfusion of affected tissues.
During hyperbaric treatment, breathing oxygen creates a strong gradient for inert gas to leave bubbles and tissues. Nitrogen or other inert gases diffuse into the circulation and are eliminated through the lungs. This promotes more rapid bubble resolution.
HBOT substantially increases the amount of oxygen dissolved in plasma. This can support tissues whose blood supply has been compromised by bubble obstruction, endothelial injury, edema, or microvascular dysfunction. This mechanism is particularly important in neurologic decompression sickness, where preservation of spinal cord or cerebral tissue may be critical to functional recovery.
Hyperbaric oxygen can produce vasoconstriction while maintaining high tissue oxygen concentrations. This combination may help reduce tissue edema without compromising oxygen availability.
DCS activates inflammatory and vascular pathways that may continue to damage tissue even after bubbles begin to resolve. Hyperbaric oxygen may influence: Leukocyte adhesion Endothelial dysfunction Inflammatory signaling Microvascular perfusion Ischemia-reperfusion mechanisms For this reason, the therapeutic effects of recompression extend beyond simply making gas bubbles smaller.
Hyperbaric or diving-medicine consultation should be obtained for suspected decompression sickness, particularly when symptoms develop following a plausible decompression exposure.
Urgent consultation is especially important for:
Even apparently mild symptoms should be discussed with a clinician experienced in diving medicine when DCS is reasonably suspected.
Recompression should generally be initiated as soon as practical when clinically indicated.
Treatment delays may allow initially reversible tissue dysfunction to progress toward permanent injury, particularly in serious neurologic decompression sickness.
However, there is no universal time cutoff after which consultation or HBOT becomes inappropriate.
Patients may present after substantial delays because:
Delayed presentation should therefore trigger individualized assessment rather than automatic exclusion from treatment.
Hyperbaric treatment for decompression sickness typically uses established recompression treatment tables rather than the shorter treatment profiles commonly used for chronic hyperbaric indications.
A commonly used initial treatment for significant DCS is the U.S. Navy Treatment Table 6 or an equivalent recompression protocol.
The appropriate treatment table is selected by the hyperbaric physician according to:
Treatment may be extended when symptoms improve incompletely during the initial recompression.
Patients with significant residual manifestations may require additional hyperbaric treatments.
The treatment strategy should be individualized by a physician experienced in diving and hyperbaric medicine.
Neurologic involvement represents one of the most consequential forms of DCS.
Spinal cord DCS may initially produce subtle symptoms such as:
These findings may progress to substantial weakness, sensory loss, bladder dysfunction, or paralysis.
A careful neurologic examination should therefore be performed and documented whenever DCS is suspected, even when the patient’s primary complaint appears to be musculoskeletal pain.
Serial examinations are valuable because neurologic findings may evolve during transport, oxygen treatment, or recompression.
Persistent neurologic deficits following initial HBOT may warrant additional recompression treatment, rehabilitation, and specialty neurologic follow-up.
Transportation decisions should be coordinated with the receiving hyperbaric or diving-medicine team whenever possible.
Additional ascent to altitude can worsen decompression stress.
For symptomatic patients, unnecessary commercial air travel or travel over significant elevations should therefore be avoided unless the transportation strategy has been specifically evaluated by the medical team.
When air evacuation is medically necessary, aircraft pressure and flight altitude become clinically relevant considerations. A pressurized aircraft capable of maintaining near-sea-level cabin pressure is preferred when available.
If transport must occur by unpressurized aircraft, flight planning should minimize altitude as safely as practical.
The safest and fastest route to definitive care depends on geography, clinical severity, transportation options, and the availability of an appropriate recompression facility.
Although recompression is the definitive therapy for DCS, patients may require additional management depending on the severity and organs involved.
Care may involve:
Patients with severe neurologic DCS may require prolonged rehabilitation even after successful recompression.
Associated diving conditions must also be considered, including:
The presence of another medical condition does not necessarily exclude DCS, as more than one dive-related injury may occur simultaneously.
Decompression sickness is recognized by the Undersea & Hyperbaric Medical Society as an accepted indication for Hyperbaric Oxygen Therapy.
Unlike many elective medical therapies, conventional randomized trials comparing recompression with no recompression are neither practical nor ethically appropriate in serious DCS because recompression has long been considered definitive treatment.
The evidence base therefore includes extensive clinical experience, observational evidence, physiologic research, military and commercial diving experience, treatment-series data, and international expert consensus.
European hyperbaric medicine consensus recommendations classify decompression illness among the conditions for which HBOT is strongly recommended.
These recommendations support:
Current diving-medicine guidance similarly identifies recompression with hyperbaric oxygen as definitive treatment for DCS.
Decompression illness is specifically listed as a covered condition under the Centers for Medicare & Medicaid Services National Coverage Determination for Hyperbaric Oxygen Therapy (NCD 20.29).
Coverage recognition does not guarantee payment for every individual treatment.
Applicable documentation, coding, medical necessity, facility, and payer requirements should be reviewed.
Consider immediate diving-medicine or hyperbaric consultation when a patient develops symptoms compatible with decompression sickness following diving, altitude exposure, or another significant decompression event.
Particular concern is warranted for:
Do not rule out decompression sickness solely because imaging is normal, the dive computer recorded no decompression violation, or symptoms improve after surface oxygen.
When DCS is suspected, early communication with an appropriate hyperbaric facility can help determine the need for recompression and coordinate safe transport.
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Moon RE. Hyperbaric oxygen treatment for decompression sickness: current recommendations. Undersea & Hyperbaric Medicine. 2019;46(5).
Moon RE. Hyperbaric oxygen for decompression sickness: 2021 update. Undersea & Hyperbaric Medicine. 2021;48(2).
Undersea & Hyperbaric Medical Society. Best Practice Guidelines: Prevention and Treatment of Decompression Sickness and Arterial Gas Embolism.
Divers Alert Network. Decompression Illness: What Is It and What Is the Treatment?
Mathieu D, Marroni A, Kot J. Tenth European Consensus Conference on Hyperbaric Medicine: recommendations for accepted and non-accepted clinical indications and practice of hyperbaric oxygen treatment. Diving and Hyperbaric Medicine. 2017;47(1):24–32.
Centers for Medicare & Medicaid Services. National Coverage Determination 20.29: Hyperbaric Oxygen Therapy.