Decompression Sickness

Decompression sickness results from bubble formation in blood and tissues when dissolved inert gas (usually nitrogen) comes out of solution during a reduction in ambient pressure, most commonly after scuba diving, but also in aviation and spaceflight. [1-2] The incidence in recreational scuba diving is 0.4–1 per 10,000 dives, but risk increases substantially with deeper, longer, or repetitive dives and decompression violations. [1]

• Dive profile details: depth, bottom time, ascent rate, number of dives that day/week, gas mixture used, compliance with dive tables or computer
• Decompression violations: missed safety stops, rapid ascent, out-of-air emergency
• Symptom onset timing: 73% of mild and 98% of severe cases present within 1 hour of surfacing; 99% within 6 hours. CNS cases present fastest — 56% within 10 minutes [1-2]
• Symptom characterization: deep boring joint pain ("the bends"), tingling/numbness (nondermatomal), weakness, vertigo, cognitive changes, rash, dyspnea, fatigue/malaise [1]
• Post-dive altitude exposure: commercial flight or mountain driving after diving can precipitate or worsen DCS — a common scenario in vacation divers [1][3]
• Important negatives: symptoms during descent or at depth are never DCS unless preceded by recent diving [2]

• Spinal cord involvement: paraparesis/paraplegia, urinary retention, girdle pain (premonitory for cord DCS) [1][4]
• Cerebral symptoms: altered consciousness, confusion, seizure, focal deficits — consider concurrent arterial gas embolism (AGE) [2]
• "The chokes": dyspnea, cough, retrosternal pain — indicates massive pulmonary vascular bubble load [1][4]
• Cardiovascular collapse: hemoconcentration, shock, coagulopathy — rare but life-threatening [1]
• Inner ear DCS: acute vertigo, nystagmus, hearing loss — more common after deep dives [1]
• Rapid symptom progression: mild symptoms can evolve into severe neurological DCS within hours [2]
• Cutis marmorata: reticular, cyanotic truncal rash — almost pathognomonic for DCS and signals systemic involvement [2]

• First-line treatment: 100% oxygen via nonrebreather or demand valve — 14% complete symptom relief, 51% symptom reduction in one large series [1]
• Adjunctive NSAIDs: tenoxicam reduced median recompression sessions from 3 to 2 in an RCT [1][5]
• IV lidocaine: considered in severe neurological AGE cases; neuroprotective in animal models but not standard of care [1-2]
• DVT prophylaxis: fractionated heparin for immobile patients with spinal cord DCS [1]
• Contraindicated: Nitrous oxide — causes bubble expansion by inward diffusion and is absolutely contraindicated [2]
• Avoid: glucose-containing IV fluids (risk of hyperglycemia worsening neurological injury), hypotonic fluids (promote intracellular edema) [2]
• Aspirin: previously advocated for antiplatelet effects but not formally studied and not recommended [2]
• Steroids: historically used but lack evidence; not standard of care [5]

• Hydration is critical: divers are often dehydrated from immersion diuresis; predive hydration reduces postdive venous gas emboli [1]
• Acute: oral noncarbonated, noncaffeinated, nonalcoholic fluids with sodium and glucose if conscious; water acceptable if nothing else available [1]
• Avoid: alcohol and carbonated beverages acutely
• Long-term: adequate hydration before and after all dives; dehydration increases DCS severity in animal models [2]

• Neurological: weakness, numbness, tingling (nondermatomal), gait instability, cognitive changes, visual disturbances, urinary retention, bowel/bladder dysfunction [1]
• Musculoskeletal: deep joint pain (shoulder, elbow, hip, knee) — present in 50–65% of cases [1]
• Vestibular/cochlear: vertigo, nausea, nystagmus, hearing loss, tinnitus [1]
• Cutaneous: rash, pruritus, mottled skin [1]
• Cardiopulmonary: dyspnea, cough, chest pain [1]
• Constitutional: fatigue, malaise, headache — present in 20–40%, often described as "viral illness" feeling [1]
• Lymphatic: truncal swelling, particularly upper chest and shoulders [1]

• Dive buddy information: corroborate dive profile, ascent rate, any in-water problems, symptom onset timing
• Dive computer data: download if available — provides objective depth-time profile
• Prior DCS episodes: history of DCS is a risk factor for recurrence [1]
• Patent foramen ovale (PFO): present in ~25–30% of adults; high-grade PFO increases DCS risk 3- to 13-fold, particularly for neurological, cutaneous, and inner ear DCS. PFO prevalence was 97.2% in divers with unprovoked DCS vs. 35.5% in controls in one study [1][6-8]
• Family history of cardiac septal defects: may suggest PFO or ASD

• Dive-related: deeper dives (>21 m), longer bottom times, rapid ascent, missed decompression stops, repetitive dives, cold water, heavy exertion during dive [1]
• Physiological: dehydration, obesity (nitrogen is more soluble in fat), older age, prior DCS, poor physical fitness [8]
• Patent foramen ovale: major independent risk factor, especially high-grade shunts [1][6]
• Post-dive altitude exposure: flying <12–18 hours after diving, mountain driving [3]
• Minimum depth threshold: DCS essentially does not occur after dives <6 m (AGE can occur at any depth) [1-2]

• Arterial gas embolism (AGE): onset typically within minutes of surfacing; altered consciousness, seizure, focal cortical signs; can coexist with DCS; treatment is the same [1-2]
• Musculoskeletal injury: shoulder/knee strain from diving activity — pain typically worsened by movement (DCS pain is not) [1]
• Inner ear barotrauma: vertigo and hearing loss from middle/inner ear pressure injury — distinguished from inner ear DCS by dive profile (barotrauma more common in shallow dives) [1]
• Stroke/TIA: focal neurological deficits — DCS typically shows nondermatomal patterns and truncal ataxia rather than classic stroke syndromes [2]
• Pulmonary barotrauma: pneumothorax, pneumomediastinum, subcutaneous emphysema — from lung overexpansion during ascent [3]
• Marine envenomation or infection: skin findings, pain
• Immersion pulmonary edema: dyspnea during or after diving
• Constitutional symptoms: seasickness, exhaustion, hypothermia, dehydration — common mimics [1]

• Prior DCS episodes: increases recurrence risk [1]
• Asthma or COPD: air trapping increases AGE risk; relative contraindication to diving [4]
• Known PFO or ASD: major risk factor [1]
• History of spontaneous pneumothorax: absolute contraindication to diving [4]
• Epilepsy, insulin-dependent diabetes: conditions impairing consciousness are contraindications [4]
• Pulmonary blebs, cysts, bullae: increase barotrauma risk [2]

• Vital signs: hypotension (hemoconcentration/shock in severe cases), tachycardia; oxygen saturation may be normal
• Complete neurological exam is essential: [1-2]
  • Mental status and cognitive testing (executive dysfunction often missed)
  • Cranial nerves (nystagmus in inner ear DCS)
  • Motor strength (paraparesis/quadriparesis)
  • Sensory exam: nondermatomal hypoesthesia is characteristic and easily missed [2]
  • Coordination: finger-nose, Romberg's sign, sharpened Romberg's test [1]
  • Gait and tandem gait (forward and backward, eyes open and closed) — truncal ataxia is common [1-2]
  • Proprioception (dorsal columns are vulnerable) [1]
• Skin: cutis marmorata (reticular cyanotic rash, truncal/proximal) — almost pathognomonic; lymphedema of trunk [2]
• Bladder: check for urinary retention (spinal cord DCS) [1]
• Joints: deep ache without local tenderness or inflammatory signs; pain unaffected by movement [1]

• DCS is a clinical diagnosis — no specific biomarkers exist [1]
• CBC/Hematocrit: hemoconcentration suggests endothelial leak and guides fluid resuscitation in severe cases [2]
• Creatine kinase (CK): elevated CK may help distinguish AGE (high in pulmonary barotrauma) from isolated DCS, though differentiation is unnecessary before recompression [2]
• BMP: assess renal function, electrolytes for fluid management
• Coagulation studies: in severe cases with suspected coagulopathy
• Labs should not delay recompression [1]

• Chest X-ray (supine) or chest ultrasound: rule out pneumothorax before recompression, especially if AGE suspected [1-2]
• MRI brain: not sensitive for acute spinal cord DCS despite significant functional impairment; corpus callosum hyperintensities on T2/FLAIR may be seen in cerebral DCS [1][9]
• CT head: not sensitive enough to rule out AGE [1]
• Imaging should NOT delay recompression unless strong suspicion of non-diving cause (e.g., cerebral hemorrhage) [2]
• Joint radiographs: bubbles rarely detectable; not useful [2]
• Bottom line: imaging is generally low-yield and should not drive the decision to recompress [1]

• Bubble contrast echocardiography (TTE with agitated saline): for PFO screening — recommended after unexplained or recurrent DCS, especially with neurological, cutaneous, or inner ear involvement [1][8]
• Transcranial Doppler with bubble contrast: alternative PFO screening method [6]
• Audiometry and electronystagmography: for inner ear DCS — can usually be deferred until after recompression [2]
• Dive computer download: objective depth-time data for risk assessment
• Divers Alert Network (DAN) hotline: 24-hour specialist consultation — (919) 684-8111 [4]

• Indications: chest pain, dyspnea, hemodynamic instability, or suspected cardiac involvement
• Possible findings: right heart strain pattern if massive venous gas emboli overwhelm pulmonary vasculature; arrhythmias if coronary AGE
• Routine ECG: reasonable in any patient with cardiopulmonary symptoms or severe DCS
• Not typically diagnostic for DCS itself but helps exclude cardiac mimics

Severity stratification is the key clinical decision point

• Mild DCS: musculoskeletal pain, cutaneous symptoms (rash, itch), constitutional symptoms (fatigue, malaise), lymphatic swelling [1]
• Serious DCS: spinal cord involvement (weakness, sensory loss, bladder dysfunction), cerebral symptoms, inner ear DCS, cardiopulmonary symptoms ("the chokes"), cardiovascular collapse [1]

Symptom onset is typically within 1–6 hours of surfacing. Presentations are often nonspecific and easily misattributed to more familiar diagnoses. The cardinal rule:

First Aid (Pre-Hospital / ED)

• Position supine (not head-down — promotes cerebral edema) [1-2]
• 100% oxygen via nonrebreather or demand valve — continue even if symptoms resolve [1-2]
• IV fluids: isotonic, glucose-free crystalloids (e.g., normal saline, lactated Ringer's); target UOP >0.5–1 mL/kg/hr. Oral rehydration if conscious and mild [1]
• Contact diving medicine specialist: DAN Emergency Hotline or local hyperbaric facility [1][4]

• Hyperbaric oxygen recompression using U.S. Navy Treatment Table 6: initial compression to 2.8 ATA breathing 100% O₂, total duration ~4 hours 45 minutes [1][5]
• Can be extended or repeated for incomplete response [1]
• Residual symptoms: daily recompressions at 2.0–2.8 ATA until resolution or plateau; most patients need only 2–3 sessions [2]
• Outcomes: 80–86% complete recovery with timely treatment; 97% complete relief when recompression is immediately available [2]
• Delayed recompression (>48 hours) still achieves 76% complete recovery — treatment should never be denied due to delay [10]

Adjunctive

• NSAIDs (e.g., tenoxicam/ibuprofen) may reduce recompression sessions needed [1][5]
• DVT prophylaxis with LMWH for immobile spinal cord DCS patients [1]

The following management algorithm from Mitchell et al. (NEJM 2022) illustrates the decision pathway for mild vs. serious DCS:

• Admit / Transfer for recompression: all serious DCS (neurological, inner ear, cardiopulmonary, cardiovascular symptoms) — urgent transfer to nearest hyperbaric facility [1]
• Mild DCS: if symptoms are static or remitting, normal neurological exam, and recompression facility is remote/inaccessible, may be managed with surface O₂ and fluids with close observation — but this decision should involve a diving medicine physician [1][3]
• Post-recompression observation: mild cases — 2 hours within reach of chamber; severe cases — 6 hours; remain within 1 hour of chamber for 24 hours [2]
• Hospital admission: for severe or residual symptoms, hemodynamic instability, or need for ongoing recompression [2]
• Helicopter transport: low altitude (<300 m / 1,000 ft); fixed-wing: pressurized to 1 atm for severe cases [2]

• Flying restrictions after DCS: [3]
  • Complete symptom relief after recompression: no flying for at least 72 hours
  • Residual symptoms: consult hyperbaric physician before any altitude exposure
• Symptom recurrence: worsening or new symptoms after treatment require immediate re-evaluation and possible repeat recompression [2]
• Return to diving: requires clearance by a diving medicine specialist; consider PFO screening (especially after neurological, cutaneous, or inner ear DCS) [1][8]
• PFO management: catheter-based PFO closure eliminated unprovoked DCS in long-term follow-up in the DIVE-PFO registry; conservative options include diving within conservative limits or cessation of diving [8][11]
• Patient counseling: educate on proper hydration, conservative dive profiles, slow ascent rates, safety stops, and avoidance of post-dive altitude exposure [3]
• Expected course: most mild cases resolve fully; spinal cord DCS may have long-term residual symptoms (numbness, bladder dysfunction, weakness) in a subset of patients [2]

1. Decompression Sickness and Arterial Gas Embolism. — Mitchell SJ, Bennett MH, Moon RE. The New England Journal of Medicine. 2022.

2. Decompression Illness. — Vann RD, Butler FK, Mitchell SJ, Moon RE. Lancet. 2011.

3. Scuba Diving: Decompression Illness and Other Dive-Related Injuries. — James Chimiak and Daniel A. Nord CDC Yellow Book. 2025.

4. Medical Problems Associated with Underwater Diving. — Melamed Y, Shupak A, Bitterman H. The New England Journal of Medicine. 1992.

5. Recompression and Adjunctive Therapy for Decompression Illness. — Bennett MH, Lehm JP, Mitchell SJ, Wasiak J. The Cochrane Database of Systematic Reviews. 2012.

6. Increased Risk of Decompression Sickness When Diving With a Right-to-Left Shunt: Results of a Prospective Single-Blinded Observational Study (The "Carotid Doppler" Study). — Germonpré P, Lafère P, Portier W, et al. Frontiers in Physiology. 2021.

7. Percutaneous Treatment of Patent Foramen Ovale and Atrial Septal Defects. — Tobis J, Shenoda M. Journal of the American College of Cardiology. 2012.

8. Screening and Risk Stratification Strategy Reduced Decompression Sickness Occurrence in Divers With Patent Foramen Ovale. — Honěk J, Šrámek M, Honěk T, et al. JACC. Cardiovascular Imaging. 2022.

9. Brain Under Pressure: Insights Into Diving-Related Lesions: A Descriptive Study. — Kouki N, Messelmani M, Moncef A, et al. Journal of the Neurological Sciences. 2025.

10. Delayed Recompression for Decompression Sickness: Retrospective Analysis. — Hadanny A, Fishlev G, Bechor Y, et al. PloS One. 2015.

11. Patent Foramen Ovale Closure Is Effective In Divers: Long-Term Results From the DIVE-PFO Registry. — Honěk J, Šrámek M, Honěk T, et al. Journal of the American College of Cardiology. 2020.