Arterial gas embolism is a potentially catastrophic condition caused by gas bubbles entering the arterial circulation, resulting in end-organ ischemia — most critically to the brain and heart. It occurs via diving-related pulmonary barotrauma or iatrogenic causes. Hyperbaric oxygen therapy (HBOT) is the definitive treatment, and early recognition is the single most important factor in improving outcomes. [1-2]
1. History
- Diving history: Depth, duration, rate of ascent, breath-holding, panic events, equipment malfunction, number of dives in the preceding days [1]
- Iatrogenic context: Recent central line placement/removal, cardiac surgery with bypass, craniotomy (sitting position), endoscopy, hemodialysis, mechanical ventilation, thoracentesis, angiography [2-4]
- Timing is critical: In divers, 92% of cases present within 5 minutes of surfacing; latency >10 minutes is rare [1]
- Symptom characterization: Sudden onset of neurologic deficits (LOC, confusion, hemiplegia, visual changes, seizures), chest pain, hemoptysis [1-2]
- Ask about prior episodes of decompression illness, pulmonary disease (asthma, COPD, bullae), and patent foramen ovale (PFO) history [1][5]
2. Alarm Features
- Sudden loss of consciousness upon surfacing or during/after a procedure (most common initial manifestation, 39%) [1]
- Acute hemiplegia, seizures, or multifocal neurologic deficits [1][6]
- Hemoptysis or chest pain suggesting pulmonary barotrauma [1]
- Cardiac arrest, cardiogenic shock, or acute ST changes (coronary AGE) [2][7]
- Cheyne-Stokes breathing, pupillary asymmetry, or respiratory/circulatory collapse [2]
- Failure to wake from anesthesia or new neurologic deficits post-procedure [1-2]
3. Medications
- 100% oxygen (FiO₂ 1.0) via non-rebreather mask or demand valve — first-line immediate treatment; promotes nitrogen washout and reduces bubble size [1-2]
- IV isotonic crystalloids (non-glucose-containing) for volume expansion, especially with hemoconcentration or shock [1]
- Avoid: Nitrous oxide (expands gas bubbles), unnecessary positive-pressure ventilation (may worsen air entrainment) [8]
- Thrombolytics are contraindicated — case reports describe fatal intracerebral hemorrhage when AGE was misdiagnosed as thromboembolic stroke [9]
- NSAIDs (e.g., tenoxicam) have shown some benefit as adjuncts to recompression in decompression sickness, though evidence is limited [1]
- Lidocaine for neuroprotection has been considered but is outside current guideline scope [7]
4. Diet
- Hydration: Divers are often dehydrated from immersion diuresis; oral noncarbonated, noncaffeinated, nonalcoholic fluids with sodium and glucose are recommended if conscious [1]
- Active predive hydration reduces postdive venous gas emboli counts [1]
- Avoid alcohol and carbonated beverages in the acute setting
- No specific long-term dietary management
5. Review of Systems
- Neurologic: LOC, confusion, focal weakness, visual changes, dysphasia, seizures, headache, dizziness [1]
- Pulmonary: Chest pain, dyspnea, hemoptysis, cough (pulmonary barotrauma) [1]
- Cardiovascular: Palpitations, chest tightness, syncope (coronary AGE) [2][7]
- Musculoskeletal: Joint pain (may overlap with decompression sickness) [1]
- Skin: Mottling, livedo reticularis (cutaneous decompression sickness)
- ENT: Vertigo, hearing loss (inner ear involvement)
6. Collateral History and Family History
- Dive buddy account of the dive profile, ascent rate, and events underwater
- Witnesses to the onset of symptoms and timeline
- History of PFO or atrial septal defect (risk for paradoxical embolism) [7]
- Prior diving injuries or decompression illness episodes
- Family history is generally not contributory unless congenital cardiac shunts are suspected
7. Risk Factors
- Diving-related: Rapid/uncontrolled ascent, breath-holding during ascent, panic, shallow-water ascent (can occur from as little as 1 m depth) [1][5]
- Pulmonary disease: Asthma, COPD, pulmonary blebs/bullae/cysts, bronchial obstruction (gas trapping) [1][5]
- Iatrogenic: Sitting-position craniotomy, cardiac surgery with bypass, CVC insertion/removal, endoscopy, hemodialysis, mechanical ventilation, thoracentesis, tissue biopsy [2-4]
- Cardiac: PFO or other right-to-left shunt (paradoxical embolism pathway) [7]
- Trauma: Penetrating thoracic injury, blast injury, pneumothorax with concurrent lung injury [8][10]
8. Differential Diagnosis
- Decompression sickness (DCS): Often indistinguishable in divers; treatment is the same; DCS typically has a more gradual onset [1]
- Thromboembolic ischemic stroke: Critical to differentiate — thrombolytics are appropriate for stroke but potentially fatal in AGE [9]
- Intracerebral hemorrhage: Sudden neurologic deficit; CT head helps differentiate
- Tension pneumothorax: May coexist with pulmonary barotrauma; must rule out before recompression [1]
- Cardiac arrhythmia / MI: Coronary AGE mimics acute coronary syndrome [2]
- Hypoglycemia, post-ictal state, near-drowning: In the diving context
- Central anticholinergic syndrome / residual anesthesia: In the postoperative setting [2]
- Fat embolism syndrome: Delayed onset (24–72 h), petechial rash, long bone fracture context [10]
9. Past Medical History
- Prior decompression illness or AGE episodes
- Pulmonary disease: asthma, COPD, bullous lung disease, prior pneumothorax
- Cardiac: PFO, ASD, other intracardiac shunts
- Recent surgeries or invasive procedures
- Seizure disorder (may confound presentation)
- Diving certification level and experience
10. Physical Exam
- Vitals: Tachycardia, hypotension (shock), bradypnea, oxygen desaturation
- Neuro: Full neurologic exam — GCS, pupillary response (asymmetry), motor/sensory deficits (often multifocal, crossing vascular territories), speech, visual fields, cerebellar signs [1][6]
- Fundoscopy: Gas bubbles in retinal vessels (pathognomonic but insensitive) [2]
- Chest: Subcutaneous emphysema, decreased breath sounds (pneumothorax/pneumomediastinum from barotrauma)
- Cardiac: Murmurs, signs of right heart failure (JVD, hepatomegaly) in massive venous embolism
- Skin: Mottling, marbling, livedo reticularis
- Increased muscle tone at the time of the event has been reported in 33% of cases [6]
11. Lab Studies
- CBC: Hemoconcentration (elevated hematocrit) from extravascular fluid shift is a nonspecific but described finding [2]
- BMP/CMP: Electrolytes, glucose (rule out hypoglycemia), renal function
- Troponin: If coronary AGE suspected [2][7]
- ABG/VBG: Assess oxygenation, ventilation, acid-base status
- Lactate: Marker of tissue hypoperfusion
- Coagulation studies: Baseline PT/INR, PTT (especially if thromboembolic stroke is in the differential)
- No specific biomarkers exist for AGE — it remains a clinical diagnosis [1]
12. Imaging
- CT head: Low sensitivity for detecting intravascular air; may show air in cerebral vessels or multifocal ischemic changes; identified free air in only 4 of 13 patients in one series [1-2][6]
- MRI brain: More sensitive; typically shows multifocal areas of restricted diffusion across multiple vascular territories (distinguishing feature from thromboembolic stroke) [6]
- Chest X-ray (supine) or chest ultrasound: Essential to rule out pneumothorax before recompression [1]
- CT chest: May show pneumomediastinum, subcutaneous emphysema, or pneumothorax from barotrauma
- Imaging should not delay definitive treatment (HBOT) [1]
13. Special Tests
- SANDHOG Criteria: Screening tool for AGE diagnosis in divers — a score ≥2 has 94.7% sensitivity and 85.7% specificity; score <2 has 100% negative predictive value [11]
- Transesophageal echocardiography (TEE): Most sensitive for detecting intracardiac air; can identify gas in cardiac chambers and assess for PFO [12]
- Transthoracic echocardiography (TTE): Can detect RV air lock or paradoxical embolism
- Precordial Doppler: Highly sensitive for venous air embolism detection (intraoperative)
- End-tidal CO₂ (ETCO₂): Sudden drop may indicate significant air embolism during procedures [12]
- Bubble study (agitated saline echocardiography): To evaluate for PFO after stabilization
14. ECG
- Indications: All patients with suspected AGE
- Coronary AGE findings: ST-segment elevation or depression, T-wave inversions (ischemia/infarction pattern) [2]
- Dysrhythmias: Bradycardia, tachycardia, ventricular fibrillation, PEA, asystole [2]
- Right heart strain: Right axis deviation, S1Q3T3, RBBB pattern (if massive venous component with RV outflow obstruction)
- Cardiac arrhythmias and myocardial suppression depend on the volume of gas embolized [2]
15. Assessment
AGE is a clinical diagnosis based on the temporal relationship between a causative event (diving ascent or invasive procedure) and the sudden onset of neurologic or cardiovascular symptoms. [1-2] Key clinical pearls:
- Symptoms are typically sudden, dramatic, and multifocal — involvement of multiple cerebrovascular territories distinguishes AGE from typical thromboembolic stroke [1]
- Spontaneous improvement occurs in ~50% of cases, but relapse is common — do not be falsely reassured [1]
- Iatrogenic AGE is frequently missed or misdiagnosed unless the clinical context is actively considered [1]
- Severity ranges from mild confusion to cardiac arrest
- Complications: persistent neurologic deficits, seizures (including status epilepticus), cerebral edema, myocardial infarction, death [6]
16. Treatment Plan
Immediate stabilization
- ABCs, standard resuscitation as needed — gas embolism does not contraindicate standard resuscitation [7]
- 100% oxygen via non-rebreather or demand valve immediately [1-2]
- Supine positioning (normal mental status) or recovery position (altered mental status); Trendelenburg is no longer routinely recommended [7]
- IV isotonic crystalloid bolus, then maintenance to target urine output >0.5–1 mL/kg/hr [1]
- Identify and stop the source of air entry (clamp lines, seal wounds) [10]
Definitive treatment
- Hyperbaric oxygen therapy (HBOT) — treatment of choice [1-2]
- U.S. Navy Treatment Table 6: initial recompression at 2.8 ATA with oxygen, typically 4–5 hours [1]
- Alternative: 2.5–3.0 ATA for 2–4 hours [4]
- Can be prolonged or repeated for poor initial response [1]
- Time to HBOT matters: probability of favorable outcome decreases from ~65% (immediate) to ~30% (15-hour delay) [13]
- HBOT ≤6 hours associated with 9-fold increased odds of favorable outcome [9]
- Delayed treatment (even up to 30–60 hours) may still provide benefit [8]
Adjuncts
- Seizure management with benzodiazepines as needed
- Aspiration of gas from the right ventricle via catheter or needle may be attempted in massive venous air embolism with cardiovascular collapse (limited evidence) [7]
- Avoid nitrous oxide, minimize positive-pressure ventilation if possible
The following figure from Mitchell et al. (NEJM 2022) illustrates the management algorithm for decompression sickness and AGE in divers:
17. Disposition
- All patients with suspected AGE require admission — there is no safe outpatient disposition
- Transfer to a hyperbaric facility as soon as cardiopulmonary stabilization is achieved [2]
- Contact Divers Alert Network (DAN) 24-hour hotline (+1-919-684-9111) or local diving medicine advisory service for guidance on nearest chamber and transport logistics [1]
- ICU admission for hemodynamic instability, cardiac arrest, severe neurologic deficits, or ongoing seizures
- Air transport: maintain cabin pressure at 1 ATA (sea level) or fly as low as safely possible to avoid further bubble expansion [1]
- Patients in cardiac arrest should receive standard CPR in the supine position; HBOT is not feasible during active arrest in most settings [7]
18. Follow Up / Return Precautions
- After HBOT: Daily recompression sessions (2.0–2.8 ATA) may be continued until symptoms resolve or plateau [1]
- Functional improvement over time is common even after severe presentations — early prognostication should be approached with caution [6]
- 26% of patients achieved modified Rankin Scale 0 at one year in one series [6]
- Return precautions: Seek immediate care for recurrence of neurologic symptoms, worsening headache, seizures, chest pain, dyspnea, or altered consciousness (relapse occurs in some patients who initially improve) [1]
- Return to diving: Requires specialist diving medicine evaluation; AGE from pulmonary barotrauma is generally considered a contraindication to further diving unless a reversible cause is identified
- Evaluate for PFO with bubble study if paradoxical embolism is suspected — PFO closure may be considered before return to diving
References
1. Decompression Sickness and Arterial Gas Embolism. — Mitchell SJ, Bennett MH, Moon RE. The New England Journal of Medicine. 2022.
2. Gas Embolism. — Muth CM, Shank ES. The New England Journal of Medicine. 2000.
3. Iatrogenic Air Embolism: Pathoanatomy, Thromboinflammation, Endotheliopathy, and Therapies. — Marsh PL, Moore EE, Moore HB, et al. Frontiers in Immunology. 2023.
4. Hyperbaric-Oxygen Therapy. — Tibbles PM, Edelsberg JS. The New England Journal of Medicine. 1996.
5. Decompression Illness. — Vann RD, Butler FK, Mitchell SJ, Moon RE. Lancet. 2011.
6. Clinical Characteristics, Imaging Findings, and Outcomes of Cerebral Air Embolism. — Brown AE, Rabinstein AA, Braksick SA. Neurocritical Care. 2023.
7. Part 10: Adult and Pediatric Special Circumstances of Resuscitation: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. — Cao D, Arens AM, Chow SL, et al. Circulation. 2025.
8. Blast Injuries. — Wolf SJ, Bebarta VS, Bonnett CJ, Pons PT, Cantrill SV. Lancet. 2009.
9. Factors Associated With Favorable Response to Hyperbaric Oxygen Therapy Among Patients Presenting With Iatrogenic Cerebral Arterial Gas Embolism. — Tekle WG, Adkinson CD, Chaudhry SA, et al. Neurocritical Care. 2013.
10. Thoracic Trauma WSES-AAST Guidelines. — Coccolini F, Cremonini C, Moore EE, et al. World Journal of Emergency Surgery : WJES. 2025.
11. Accuracy of a SET of Screening Parameters Developed for the Diagnosis of Arterial Gas Embolism: The SANDHOG Criteria. — Hayden SR, Buford KC, Castillo EM. The Journal of Emergency Medicine. 2015.
12. Transesophageal Echocardiography Detection of Air Embolism During Endoscopic Surgery and Validity of Hyperbaric Oxygen Therapy: Case Report. — Guo JL, Wang HB, Wang H, et al. Medicine. 2021.
13. Early Hyperbaric Oxygen Therapy Is Associated With Favorable Outcome in Patients With Iatrogenic Cerebral Arterial Gas Embolism: Systematic Review and Individual Patient Data Meta-Analysis of Observational Studies. — Fakkert RA, Karlas N, Schober P, et al. Critical Care. 2023.