Pulmonary Barotrauma & AGE

Pulmonary Barotrauma and Arterial Gas Embolism

Pulmonary barotrauma (PBT) occurs when expanding gas inside the lungs cannot escape during ascent and the resulting pressure differential exceeds the mechanical limits of lung tissue. The cause, in almost every case, is a closed or partially closed airway during ascent — breath-holding being the most common scenario.

Boyle's Law describes the mechanism: as ambient pressure decreases during ascent, gas volume increases proportionally. A diver who surfaces from 10 m with a full breath held undergoes a doubling of lung gas volume — enough to cause serious injury if the glottis is closed.

The critical pressure threshold for alveolar rupture is approximately 70–80 mmHg transpulmonary pressure (Hills 1993; Germonpré et al 2008). Even small depth changes can generate this differential. A diver holding a breath during an ascent of just 1–2 m, if the lung is already at full volume, can produce enough overexpansion to rupture alveolar tissue.

Pre-existing lung conditions — bullae, cysts, subpleural blebs, severe asthma with air trapping — reduce the pressure threshold further. But published case series consistently document PBT in divers with structurally normal lungs and normal chest X-rays (van Hulst & van Ooij 2024; Germonpré et al 2008; Acott 2002). The primary cause in these cases is always a compromised airway during ascent.

When alveoli rupture, gas escapes into surrounding structures: pneumothorax (gas enters the pleural space, potentially collapsing the lung); mediastinal emphysema (gas tracks along tissue planes into the mediastinum); or subcutaneous emphysema (gas migrates to tissues under the skin of the neck and chest). These presentations range from clinically benign to immediately fatal.

How Arterial Gas Embolism Occurs

If ruptured alveoli are adjacent to pulmonary veins, gas can enter the pulmonary venous circulation and be carried directly into arterial blood. The sequence: breath held during ascent; transpulmonary pressure exceeds ~70–80 mmHg; alveolar rupture; gas enters pulmonary veins, then left atrium, left ventricle, and systemic arterial circulation; bubbles obstruct cerebral, coronary, or spinal arteries.

Arterial gas embolism (AGE) produces neurological symptoms within minutes of surfacing — before any decompression sickness mechanism could be active. The presentation is stroke-like: sudden loss of consciousness, seizures, hemiplegia, visual loss, profound confusion. Coronary involvement can cause ventricular arrhythmia or arrest.

AGE is one of the few diving emergencies where the window between injury and irreversible damage is measured in minutes, not hours.

Who Is at Risk

Any diver ascending while breath-holding — even from shallow depths — is at risk. Panicked divers who arrest breathing under stress or when low on gas. Divers with pulmonary air trapping (asthma, bullae, cysts), regardless of whether these were declared at medical screening. Incorrect dry suit inflation technique that restricts thoracic expansion on ascent. Out-of-air emergencies with rapid buoyant ascents.

Healthy lungs are not immune. The structural integrity of the alveoli is not the limiting factor when a full-volume breath is held through a significant pressure change — the physics of gas expansion will produce rupture regardless.

Presentations

Pulmonary barotrauma may present with sharp chest pain during or immediately after ascent, coughing up frothy or blood-tinged sputum, dyspnoea, reduced oxygen saturation, or crackling crepitus under the skin of the neck and chest.

Arterial gas embolism typically presents within minutes of surfacing: sudden loss of consciousness or altered mental status, seizure, focal neurological deficit (unilateral weakness, speech impairment, visual disturbance), or cardiovascular collapse if coronary involvement.

Differential Diagnosis

Three conditions produce acute neurological symptoms in divers after surfacing, and distinguishing them matters because the mechanisms differ even though first-line treatment (100% oxygen, recompression) overlaps.

AGE presents within minutes of surfacing, almost always associated with a breath-hold or panic ascent. The rapidity of onset and the history of airway compromise are the key distinguishing features. No significant decompression exposure is required.

Neurological DCS (Type II) typically presents 30 minutes to 2 hours after surfacing, following a dive with sufficient inert gas loading. A history of deep or repetitive dives with inadequate decompression is typical.

Cervical arterial dissection is a less common but important differential. Pollock et al (2024) reviewed 19 reported cases of arterial dissection in scuba divers, 14 involving cervical or intracranial arteries. Mean age was 44 years. Contributing factors included immersion-related vasoconstriction and blood redistribution (the mammalian dive response), which generates significant increases in aortic and cervical arterial wall stress, combined with pre-existing hypertension, equipment posture, and increased work of breathing at depth. Cervical arterial dissection produces stroke-like neurological symptoms that can develop during or after a dive and may be misattributed to DCS or AGE. The diagnosis requires vascular imaging (CT angiography or MRI) and is typically missed on clinical examination alone.

From the DAN 2018 differential diagnosis workshop: DCI is a clinical diagnosis with no confirmatory test. Imaging should not delay recompression when DCI is clinically suspected, but cervical dissection should remain on the differential when neurological symptoms persist after HBO treatment or when the clinical picture does not fit the usual DCI pattern.

Inner Ear Presentations: An Important Distinction

Inner ear DCS (IEDCS) and inner ear barotrauma (IEBt) both produce cochleovestibular symptoms — vertigo, nausea, hearing loss, tinnitus — but through entirely different mechanisms and with different optimal treatments.

Lindfors et al (2021), in a systematic review of 25 IEBt studies (n=183) and 18 IEDCS studies (n=397), identified the key differentiators. IEBt arises from mechanical damage caused by a middle-to-inner ear pressure gradient during descent. The predominant symptom is cochlear — hearing loss and tinnitus — with vestibular symptoms less prominent; more common in freediving. IEDCS arises from bubble formation within the membranous labyrinth or from arterialised venous bubbles reaching the labyrinthine artery. The predominant symptom is vestibular — true rotational vertigo, nausea, nystagmus — onset during or after ascent, typical after deeper SCUBA dives (mean depth ~43 msw in the reviewed studies vs ~13 msw for IEBt).

Treatment diverges: IEDCS requires urgent HBOT. IEBt may require surgical management (perilymph fistula repair) or conservative management, and HBOT is not the primary intervention. Misclassification delays appropriate care and worsens outcomes.

Prevention

The single most effective prevention is an open airway during ascent: continuous passive exhalation while ascending (not forced, not held); controlled ascent rate no faster than 9–10 m/min; never breath-holding on the surface before a free ascent or during a buoyant emergency. If ascent is uncontrolled, the priority is airway — exhale.

Pre-dive medical screening for undeclared pulmonary conditions reduces risk in the subset of divers with pre-existing pathology. But the majority of PBT/AGE cases occur in structurally normal lungs — no screening eliminates the risk of a breath-hold ascent.

Emergency Response

1. Remove the diver from the water and position supine — horizontal positioning prevents pooling of arterial bubbles in the cerebral circulation
2. Administer 100% oxygen continuously via tight-fitting non-rebreather mask
3. Do not give aspirin if AGE is suspected (intracranial bleeding risk)
4. Call DAN emergency line and local emergency services simultaneously
5. Evacuate to the nearest hyperbaric facility — recompression using US Navy Treatment Table 6 (2.8 ATA) is standard for AGE
6. Do not delay evacuation while waiting for symptom improvement — AGE can produce transient apparent recovery followed by deterioration

Time to recompression is the primary determinant of neurological outcome.

References

• Hills BA (1993). Analysis of underwater barotrauma thresholds. Referenced in Germonpré et al 2008.
• Germonpré P, Balestra C, Vanmaele P (2008). Pulmonary barotrauma. Diving and Hyperbaric Medicine.
• Acott CJ (2002). Pulmonary barotrauma case series. South Pacific Underwater Medicine Society Journal.
• van Hulst RA, van Ooij PJAM (2024). Pulmonary barotrauma in diving. Diving and Hyperbaric Medicine.
• Price DL et al (2021). Pneumomediastinum in divers. Referenced in DHM literature.
• Lindfors OH, Räisänen-Sokolowski AK, Hirvonen TP, Sinkkonen ST (2021). Inner ear barotrauma and inner ear decompression sickness: a systematic review on differential diagnostics. Diving and Hyperbaric Medicine 51(4):328–337. doi:10.28920/dhm51.4.328-337
• Pollock NW, Lippmann J, Pearn J, Hayman J (2024). Arterial dissection in scuba divers: a potential adverse manifestation of the physiological effects of immersion. Diving and Hyperbaric Medicine 54(3):188–195. doi:10.28920/dhm54.3.188-195
• Denoble PJ, Marroni A (eds) (2019). Differential Diagnosis of Decompression Illness Workshop Proceedings. DAN/UHMS.

Related Reading

• Decompression Sickness

• Predisposing Factors for DCS

• Thermal Stress in Diving

• Immune Suppression and Diving

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