Definition and epidemiology
Decompression sickness is a syndrome caused by the formation and growth of inert gas bubbles (primarily nitrogen, sometimes helium in technical diving) within blood vessels and tissues when a diver or other individual undergoes too rapid a reduction in ambient pressure. The gas, dissolved under high pressure, comes out of solution faster than it can be eliminated through the lungs, forming bubbles analogous to the fizz released when a soda bottle is opened.
- Occurs almost exclusively in scuba and compressed-air divers, but also in high-altitude aviators, astronauts during extravehicular activity, and caisson/tunnel workers transitioning from high-pressure environments.
- Estimated incidence in recreational scuba diving is roughly 2-4 cases per 10,000 dives, though this varies with dive profile, depth, and ascent rate.
- Risk increases with dive depth, dive duration, rapid ascent, multiple dives in a short period, cold water, dehydration, obesity, and flying soon after diving.
- Two classic clinical patterns are described: Type I (mild, musculoskeletal/cutaneous) and Type II (serious, neurologic/cardiopulmonary).
- Caused by nitrogen bubble formation after rapid ascent from depth, not by lung overexpansion (that is arterial gas embolism).
- Type I = joint pain and skin findings; Type II = neurologic, pulmonary, or inner ear involvement.
- Spinal cord DCS classically affects the lower thoracic/lumbar cord due to venous drainage patterns.
- 100% oxygen is first aid; hyperbaric recompression is the definitive treatment for all significant cases.
- Do not delay transport to a hyperbaric chamber for imaging or labs; diagnosis is clinical.
- PFO increases risk of serious/paradoxical DCS by allowing venous bubbles into arterial circulation.
- Avoid flying for 12-24+ hours after diving to prevent symptom provocation.
- Dysbaric osteonecrosis of femoral/humeral heads is a long-term complication of repeated bubble-related ischemia.
Etiology and risk factors
The underlying cause is a reduction in ambient pressure that is too rapid relative to the amount of inert gas dissolved in blood and tissue, exceeding the rate at which it can be off-gassed safely through the lungs.
Risk factors
- Rapid or uncontrolled ascent, or omission of required decompression stops
- Deep dives, long bottom times, repetitive dives within short intervals
- Flying within 12-24 hours after diving (reduced ambient pressure at altitude)
- Cold water exposure (reduces peripheral perfusion and gas elimination)
- Dehydration, exertion during or after the dive
- Obesity (nitrogen is more soluble in fat, increasing total body nitrogen load)
- Patent foramen ovale (PFO) or other right-to-left shunt, allowing venous bubbles to bypass pulmonary filtration and reach the arterial circulation
- Older age, poor physical fitness
- Breathing gas with higher inert gas fraction (e.g., standard air versus enriched oxygen mixtures)
Pathophysiology
During descent, increased ambient pressure drives more inert gas (mainly nitrogen) into solution in blood and tissues according to Henry's law. During ascent, if pressure is released too quickly, the gas cannot diffuse out through the lungs fast enough and instead forms bubbles directly within tissues and the venous (and sometimes arterial) circulation.
- Bubbles can form locally in tissues (autochthonous bubbles), causing mechanical distention and pain, classically in joints ("the bends").
- Venous gas emboli travel to the lungs; small numbers are usually filtered and exhaled, but large bubble loads can overwhelm pulmonary filtration.
- In the presence of a PFO or atrial septal defect, venous bubbles can cross into the arterial circulation, causing systemic embolization to the brain, spinal cord, or inner ear.
- Bubbles trigger a secondary inflammatory cascade: endothelial injury, platelet activation and aggregation, complement activation, and capillary leak, which worsens tissue ischemia independent of the mechanical bubble effect.
- Spinal cord DCS preferentially affects the lower thoracic and lumbar cord, thought to relate to the venous drainage pattern (Batson's plexus) and relatively sluggish perfusion in that region.
Clinical features
Symptoms typically begin within minutes to 24 hours after surfacing, with most cases presenting within the first 6 hours.
Type I (mild)
- Joint and limb pain ("the bends"), classically a dull ache in shoulders, elbows, or knees
- Skin manifestations: itching, mottled or marbled rash (cutis marmorata), subcutaneous emphysema
- Lymphatic involvement: localized swelling
Type II (serious)
- Neurologic: paresthesias, weakness, paraplegia or paraparesis (spinal cord DCS), ataxia, confusion, visual disturbances
- Inner ear ("the staggers"): vertigo, tinnitus, hearing loss, nausea/vomiting
- Pulmonary ("the chokes"): dyspnea, chest pain, cough, from pulmonary vascular gas embolism; can progress to respiratory failure
- Cardiovascular: hypotension, shock from massive gas embolism (rare, severe)
Arterial gas embolism (AGE) is a related but distinct, more immediate entity caused by pulmonary barotrauma (lung overexpansion) rather than nitrogen bubble formation; it presents within minutes of surfacing with stroke-like focal neurologic deficits or loss of consciousness.
Diagnosis
Diagnosis is clinical, based on a history of diving (or other pressure exposure) followed by a compatible symptom onset. No single laboratory or imaging test confirms DCS, and treatment should not be delayed for confirmatory testing.
- Detailed dive history: depth, duration, ascent rate, number of repetitive dives, use of decompression stops, and timing of symptom onset relative to surfacing
- Full neurologic examination to detect subtle deficits (common in spinal and cerebral DCS)
- Pulse oximetry and chest exam to evaluate for pulmonary involvement
- MRI of the brain or spinal cord may show lesions in severe neurologic DCS but is often normal early and should not delay recompression
- Echocardiography (with bubble study) can be used after the acute event to evaluate for PFO if recurrent DCS or unprovoked serious DCS occurred
- Chest X-ray if pulmonary symptoms or suspected pneumothorax/barotrauma
- Diagnosis is essentially a clinical diagnosis of exclusion combined with a supportive context; a therapeutic response to recompression can retrospectively support the diagnosis
Differential diagnosis
| Condition | Distinguishing feature |
|---|---|
| Arterial gas embolism | Immediate onset (seconds to minutes) after surfacing, often with loss of consciousness; due to pulmonary barotrauma, not slow bubble formation |
| Musculoskeletal strain/injury | No bubble pathophysiology; pain reproducible with movement, no systemic or neurologic signs |
| Spinal cord compression (disc, trauma) | No diving/pressure exposure history; imaging shows structural lesion |
| Stroke (ischemic/hemorrhagic) | Can mimic cerebral DCS; distinguished by dive history and bilateral or patchy spinal findings in DCS |
| Immersion pulmonary edema | Occurs during the dive itself, not after ascent; presents with dyspnea and pink frothy sputum |
| Marine envenomation | Local sting/contact history, no relation to ascent rate or dive profile |
| Hypothermia | Diving-related but due to cold exposure; confusion and shivering rather than focal neurologic signs |
Management
All suspected DCS cases should be treated promptly; the threshold for treatment is low because delayed therapy worsens neurologic outcomes.
Immediate (first aid)
- Administer 100% supplemental oxygen by tight-fitting mask as soon as possible, continued during transport
- Position the patient supine (the old head-down/Trendelenburg position is no longer recommended)
- Oral hydration if the patient is conscious and able to swallow; IV isotonic fluids if available and the patient is impaired
- Arrange urgent transport to the nearest hyperbaric chamber; air transport should be at the lowest safe altitude or in a pressurized cabin
Definitive treatment
- Hyperbaric oxygen therapy (recompression) is the definitive treatment for all but the most trivial cases: it mechanically reduces bubble size, improves oxygenation of ischemic tissue, and reduces the inflammatory cascade
- Standard treatment protocols (e.g., US Navy Treatment Table 6) use recompression to a set depth equivalent with oxygen breathing, followed by gradual, controlled decompression
- Repeat hyperbaric sessions may be needed for residual or worsening neurologic deficits
- Adjunctive IV fluids to maintain hydration and perfusion
- Analgesics for joint pain, avoiding agents that might mask evolving neurologic signs until the patient has been evaluated
- Lidocaine infusion has been studied as adjunctive therapy in some severe neurologic cases but is not standard first-line therapy
Prevention and follow-up
- Adherence to established dive tables or dive computer algorithms, with conservative ascent rates and safety stops
- Avoiding flying for at least 12-24 hours after diving (longer after multiple or deep dives, per diving medicine society guidance)
- Divers with unprovoked serious DCS, or recurrent DCS, may be evaluated for PFO; closure can be considered on a case-by-case basis, though this is not universally recommended for all divers with incidental PFO
- Fitness-to-dive evaluation after a DCS episode, typically with a diving medicine specialist
Complications and prognosis
Most Type I (mild musculoskeletal) DCS resolves completely with prompt oxygen and recompression therapy. Outcomes for Type II (neurologic) DCS depend heavily on how quickly recompression is initiated.
- Residual neurologic deficits (weakness, sensory loss, bladder/bowel dysfunction) can persist, particularly with delayed treatment or severe spinal cord involvement
- Chronic inner ear damage (hearing loss, persistent vertigo) may occur with inadequately treated inner ear DCS
- Dysbaric osteonecrosis is a long-term complication from repeated or severe bubble-related ischemia to bone, typically affecting the femoral or humeral heads
- Recurrent DCS risk is increased in divers with untreated PFO or those who continue high-risk diving practices
- Overall mortality is low when treatment is prompt, but severe pulmonary or cardiovascular DCS (massive gas embolism) carries significant mortality risk if recompression is delayed
Think "BENDS": Bubbles, Elevated risk with rapid ascent, Nitrogen the culprit gas, Dive history is key, Send to hyperbaric chamber.
Practice questions
1. A 34-year-old man develops dull pain in both shoulders and an itchy, mottled rash on his trunk 2 hours after completing a deep recreational scuba dive with a rapid ascent. He is alert, oriented, and has a normal neurologic exam. Which of the following is the most appropriate immediate step?
2. A 29-year-old woman surfaces after a 40-minute dive to 30 meters with a rapid, uncontrolled ascent due to equipment malfunction. Thirty minutes later she develops bilateral leg weakness, numbness below the umbilicus, and urinary retention. Which structure is most likely affected by this process?
3. A 41-year-old recreational diver is found to have recurrent episodes of decompression sickness despite following conservative dive tables and ascent rates. Which underlying condition should be evaluated as a potential contributing risk factor?
Frequently asked questions
What causes decompression sickness?
Decompression sickness is caused by nitrogen gas coming out of solution and forming bubbles in blood and tissue when a diver ascends too quickly after breathing compressed air at depth. The faster the ascent relative to the amount of dissolved nitrogen, the greater the bubble formation. Risk is increased by deep or long dives, repetitive dives, cold water, dehydration, and flying soon after diving.
What are the first symptoms of decompression sickness?
The earliest symptoms are usually joint or limb pain, often described as a dull ache, along with itching or a mottled skin rash. These typically appear within minutes to several hours after surfacing. More serious cases can also present early with numbness, weakness, dizziness, or shortness of breath, which signal neurologic or pulmonary involvement requiring urgent treatment.
How is decompression sickness diagnosed?
Decompression sickness is diagnosed clinically, based on a recent diving (or pressure exposure) history combined with compatible symptoms such as joint pain or neurologic deficits. There is no definitive blood test or imaging study, though MRI may later show spinal or brain lesions in severe neurologic cases. Treatment with oxygen and recompression is started immediately without waiting for confirmatory tests.
Is decompression sickness curable?
Yes, most cases resolve completely with prompt treatment using 100% oxygen followed by hyperbaric recompression therapy. Outcomes are best when treatment begins quickly after symptom onset. Delayed treatment, especially in neurologic (Type II) cases, increases the risk of permanent deficits such as weakness, sensory loss, or hearing loss.
Decompression sickness vs arterial gas embolism — what is the difference?
Decompression sickness results from slow nitrogen bubble formation in tissues after a too-rapid ascent, with symptoms developing over minutes to hours. Arterial gas embolism results from lung overexpansion (barotrauma) during ascent, forcing air directly into the arterial circulation, causing immediate stroke-like symptoms or collapse within seconds to minutes of surfacing. Both are treated with oxygen and emergency recompression.
Key drugs
Related conditions and differentials
Sources and further reading
StatPearls (NCBI Bookshelf)MedlinePlusWHO ICD-10: T70.3
Educational content for medical students, prepared by the WhiteCoat Pro editorial team with AI assistance; every page is reviewed by a second AI model for factual errors. It is not medical advice and does not replace the product label, local guidelines or a clinician.