Arterial gas embolism or neurological decompression sickness

A 41-year-old astronaut trains extravehicular activity in a neutral buoyancy pool, wearing the pressurized suit and breathing compressed gas. During the ascent, an equipment problem forces her back to the surface faster than planned. She arrives conscious, speaks with the team and, in less than five minutes, stops responding. When she opens her eyes again, she is confused and does not move her left arm and leg well. The scene is fictional and was written for teaching.

This text uses the scene as a setting for clinical reasoning. The central question seems academic, but it changes the initial approach little and the reasoning a lot: did the gas reach the cerebral arteries through a ruptured lung, or did it form in the tissues because dissolved inert gas came out of solution? The text is not a summary of diving rules or of space agencies. If you play the case of the day on NEXO, you will recognize the challenge: the clock between the ascent and the first symptom is as strong a clue as any exam.

Key points

• A neurological symptom within 10 minutes after surfacing suggests arterial gas embolism.
• Neurological decompression sickness usually starts later and with spinal signs.
• The diagnosis is clinical and recompression does not wait for confirmation.
• A normal image does not rule out arterial gas embolism.
• Oxygen at the highest possible fraction is the first aid in both conditions.
• Associated pneumothorax must be considered before the chamber.

Why this is a reasoning scenario

The case combines an uncommon environment, a rapid event and a neurological deficit that resembles a stroke. Both hypotheses arise from gas in the wrong place when the ambient pressure falls. A review on treatment describes that gas enters the arteries through a rupture between alveolus and capillary, as in an ascent with breath held, or forms in the veins from bubbles in the tissues during decompression, in diving or in exposure to altitude (Moon, 2019).

Pool training seems safe because the depth is small. The US Navy diving manual undoes this idea: any diver who breathed compressed gas, even in a pool, and who surfaces unconscious or loses consciousness shortly afterward must be treated as having arterial gas embolism (US Navy Diving Manual, Revision 7). The reasoning therefore starts from the exposure, not from the depth.

What the scene teaches

The astronaut brings three clues that weigh together. She breathed compressed gas, ascended fast and lost consciousness within minutes. Each clue alone suggests little, but the combination changes the probability greatly. The post on signs, symptoms and history shows how the temporal sequence of the account can be worth more than an isolated finding.

Two diseases, one same gas

Arterial gas embolism happens when alveolar gas enters the arterial circulation (Moon, 2019). The best-known path is lung rupture during an ascent with breath held. The gas can also come from venous bubbles that pass to the arterial side through a cardiac shunt or through the pulmonary vessels themselves. Decompression sickness, on the other hand, is caused by bubbles formed in the tissue itself from dissolved inert gas.

A review on treatment describes that arterial gas embolism generally produces manifestations similar to those of a stroke, such as altered consciousness, confusion, seizures and focal deficits (Moon, 2019). The author notes that small amounts of venous gas are usually filtered by the lung capillaries, but that this gas can reach the arteries by passing through the lung or through a patent foramen ovale.

The same event in another environment

The clock as the main clue

The US Navy manual gives time a central role. Arterial gas embolism usually begins within 10 minutes of reaching the surface, and the manual recommends observing the diver for that period (US Navy Diving Manual, Revision 7). If pain is the only symptom, arterial gas embolism is unlikely.

Decompression sickness has a more spread-out onset over time. According to the same manual, about 42 in every 100 begin in the first hour after surfacing, 60 within 3 hours, 83 within 8 hours and 98 within 24 hours (US Navy Diving Manual, Revision 7). A symptom that appears an hour after the dive does not rule out decompression sickness, but it makes arterial gas embolism less likely.

A series of 5278 episodes of decompression sickness in commercial fishing divers, treated at a single hyperbaric center, points in the same direction: the first symptom appeared within 6 hours in almost all of them, with a median of 62 minutes, and the shorter the latency, the more severe the condition (Xu and colleagues, 2012).

The overlap that confuses

The manual notes that type II decompression sickness, which includes the neurological forms, and arterial gas embolism have very similar symptoms (US Navy Diving Manual, Revision 7). For this reason, the text asks that treatment not be delayed in order to confirm the diagnosis. In this case, the time of a few minutes and the loss of consciousness point to arterial gas embolism, but the immediate approach would be the same if the hypothesis were neurological decompression sickness.

Neurological decompression sickness: the other side

The neurological form of decompression sickness has its own presentation. The manual describes paresthesias, weakness and urinary changes, and warns that divers often deny or minimize symptoms at the start (US Navy Diving Manual, Revision 7). A tingling that climbs up the legs an hour after the dive, with difficulty urinating, tells a different story from a sudden loss of consciousness.

The pattern of the injury helps. Arterial gas embolism usually produces cerebral signs, while neurological decompression sickness often affects the spinal cord, with band-like or bilateral symptoms. The two can coexist, and diving or training with a lot of accumulated inert gas increases the chance of venous bubbles that later cross to the arterial side.

Clue	Favors arterial gas embolism	Favors neurological decompression sickness	Source
Onset	Within 10 minutes of surfacing	In the first hour or later	US Navy Diving Manual
Pattern	Similar to stroke, altered consciousness	Paresthesias, weakness, urinary changes	US Navy Diving Manual
Isolated pain	Makes the hypothesis unlikely	Compatible with non-neurological forms	US Navy Diving Manual
Normal imaging	Can occur anyway	Can occur anyway	Moon, 2019
First aid	Oxygen and recompression	Oxygen and recompression	Moon, 2019

Pathophysiology: from Boyle to the cerebral artery

In arterial gas embolism, the starting point is Boyle's law. When the pressure around the lung falls during ascent, gas trapped in the alveoli expands. If the exit is blocked, by breath-holding or by a region of trapped air, the first step is rupture of the alveolus, and the gas can travel to the pleura or to the arterial circulation, with greater risk in the arteries of the brain and heart (US Navy Diving Manual, Revision 7).

The damage is not only mechanical. Moon's review describes that intravascular gas can obstruct arteries or injure the endothelium, with secondary vasospasm and capillary leakage (Moon, 2019). This helps explain why the condition can improve when the bubble passes and then worsen again.

The lung that already had a flaw

In France, chest CT has replaced radiography in the initial assessment of candidates for military diving since 2018. In a study of 307 candidates, air-containing lesions such as cysts and bullae were far less frequent than benign nodules, but they generally led to disqualification, and the authors advocate screening for these lesions in professional divers (Bonnemaison and colleagues, 2022).

Even so, they appear in healthy people. In a CT study of young adults without lung disease, bullae or blebs were present in 7.2 out of every 100 people up to age 40, and age, male sex and smoking were independent risk factors (Bresser and colleagues, 2024). For reasoning, this means that an apparently normal lung can have the weak spot that allows rupture.

In decompression sickness, the gas comes from within

In decompression sickness, the story is different. At depth, blood and tissues absorb more nitrogen. If the ascent is too fast, this excess gas comes out of solution and forms bubbles, with mechanical and biochemical effects (US Navy Diving Manual, Revision 7).

In astronaut training, the breathing mixture is chosen to reduce this risk. In the American agency's neutral buoyancy laboratory, the suit uses a mixture with 46 parts oxygen per 100 to limit the partial pressure of nitrogen, with the trade-off of greater oxygen exposure (Walker and colleagues, 2018). Over 20 years of training, the authors recorded no case of oxygen toxicity in the nervous system. The mixture reduces the risk of decompression sickness, but it does not protect the lung from a rapid ascent.

The role of patent foramen ovale

Right-to-left shunt is the bridge between the two diseases. A recent review estimates that patent foramen ovale is present in about one in four adults and links it to decompression sickness (Meng and colleagues, 2026). Through it, venous bubbles that would be filtered in the lung can reach the arteries and produce an arterial picture from decompression sickness.

The same review recommends shunt testing for selected, high-risk people, not screening everyone (Meng and colleagues, 2026). The methods cited are transthoracic echocardiography with microbubble contrast and transcranial Doppler. The text does not recommend routine closure as primary prevention. In the astronaut's case, this investigation belongs to follow-up, not to initial care.

Why this question comes later

Knowing whether there is a shunt helps explain the event and plan the return to training, but it does not change what to do in the first minutes. The post on clinical decision-making discusses exactly this order: a test is useful when the answer changes the next step. In initial care, the bubble echocardiogram changes nothing. Later, it can change a lot.

The differential diagnosis

Loss of consciousness followed by hemiparesis has other causes, and the reasoning must go through them without delaying treatment. The hypotheses the scene requires considering are:

• Arterial gas embolism from pulmonary barotrauma.
• Neurological decompression sickness, cerebral or spinal.
• Ischemic or hemorrhagic stroke unrelated to the exposure.
• Hypoglycemia, which can mimic a focal deficit.
• Seizure with postictal deficit.
• Oxygen toxicity, in training with enriched mixtures.
• Immersion pulmonary edema, if there is shortness of breath or cough after training.

Hypoglycemia is the easiest to check and one of the most dangerous to forget, because capillary blood glucose takes seconds. A seizure with postictal deficit may be a manifestation of the embolism itself, not an alternative to it. Oxygen toxicity enters the differential because of the use of an enriched mixture, but the American laboratory series recorded no adverse neurological event (Walker and colleagues, 2018). Immersion pulmonary edema was first described in divers with shortness of breath after dives in open sea and cold water, and it can occur in young, healthy people (Tetzlaff, Swenson and Bärtsch, 2022).

The trap of improvement

If the astronaut improves in the following minutes, the temptation is to conclude that it was a scare. The US Navy manual insists that treatment should not wait for the diagnosis (US Navy Diving Manual, Revision 7), and Moon's review explains the risk: in cerebral embolism, an apparent improvement can be followed by worsening hours later, and so early chamber treatment is recommended even for those who seem to have recovered on their own (Moon, 2019). The post about diagnostic pause shows how to build the habit of reviewing before concluding.

Tests: what helps and what delays

The diagnosis is clinical. Moon's review states that vascular gas often does not appear on imaging and that imaging should not be used to rule out arterial gas embolism (Moon, 2019). A normal head CT, therefore, does not keep the astronaut out of the chamber.

The US Navy manual recalls, however, that an associated pneumothorax cannot go unnoticed (US Navy Diving Manual, Revision 7). The alveolar rupture that carried gas to the arteries can also carry gas to the pleura. An undrained pneumothorax can grow dangerously during the decompression phase in the chamber, and so chest examination is part of the assessment before or during recompression.

Quick tests that change management

• Capillary glucose, to rule out hypoglycemia.
• Repeated neurological examination, to follow the course.
• Chest examination and imaging as available, looking for pneumothorax.
• Assessment of urine output, which guides fluid replacement.

The post about pretest probability helps to understand why a normal test changes little when the initial probability is high. In the astronaut, the combination of compressed gas, rapid ascent and loss of consciousness within minutes leaves the probability of arterial gas embolism so high that a normal image does not bring it down.

Initial management and recompression

First aid is 100 percent oxygen, and the definitive treatment is recompression while breathing oxygen (Moon, 2019). The US Navy manual calls for surface oxygen in all cases, by reservoir mask at a flow of 15 L/min or by demand valve, and states that it is usually tolerated for up to 12 hours (US Navy Diving Manual, Revision 7). The same manual calls for the patient to lie down and for immediate recompression after securing airway, breathing and circulation.

Table 6

Table 6 of the US Navy is indicated for arterial gas embolism and for type II decompression sickness (US Navy Diving Manual, Revision 7). It starts at 60 feet of seawater, about 18 meters, with 20-minute oxygen periods separated by 5 minutes of air, and lasts 4 hours and 45 minutes without extensions. The manual allows extending the table by up to 2 oxygen periods at 60 feet and 2 at 30 feet, depending on the response. The choice of table and extensions belongs to the hyperbaric medicine physician.

Time to the chamber also matters. In a meta-analysis of cerebral arterial gas embolism caused by medical procedures, the chance of a good outcome fell from about 65 in 100, with the chamber started right away, to about 30 in 100 with a 15-hour delay (Fakkert and colleagues, 2023). The context is hospital, not diving, but the lesson for the case is the same: do not wait.

For mild cases of decompression sickness, research also compares shorter tables. A randomized clinical trial compared two treatment tables in the initial management of mild decompression sickness (Banham and colleagues, 2022). This type of study does not apply to a picture with loss of consciousness and hemiparesis, which is severe by definition.

Fluids, position and what to avoid

The manual recommends isotonic fluids without glucose in decompression sickness, but calls for caution with overload in arterial gas embolism, because of the risk of cerebral edema, and suggests monitoring urine output with a target of 0.5 mL/kg/h (US Navy Diving Manual, Revision 7). The text does not recommend corticosteroids, and antiplatelet agents and anticoagulants are not routine. When there is brain or spinal cord injury, the manual also calls for strict treatment of raised temperature.

Hyperventilation to reduce intracranial pressure seems logical, but it has no support. Moon reports that animal studies showed no benefit of induced hypocapnia in cerebral arterial gas embolism, despite frequent intracranial hypertension (Moon, 2019).

Adjuvant therapies and doses

Venous thromboembolism prophylaxis is recommended for those who become paralyzed. The US Navy manual specifies enoxaparin 30 mg subcutaneously every 12 hours for those who cannot walk due to lower limb paralysis (US Navy Diving Manual, Revision 7).

Lidocaine has weaker evidence. The US Navy manual classifies it as potentially beneficial in arterial gas embolism, with 1 mg/kg IV followed by an infusion of 2 to 4 mg/min, only under medical supervision, and does not recommend it in decompression sickness (US Navy Diving Manual, Revision 7).

What the evidence has not yet settled

The manual calls lidocaine only potentially beneficial and warns that higher doses can cause paresthesias, ataxia and seizures (US Navy Diving Manual, Revision 7). For reasoning, the lesson is to separate what is central, oxygen and recompression, from what is adjuvant and uncertain.

Reasoning: what remains from the case

The scenario teaches you to give time the weight it deserves. The question "when did it start relative to the ascent?" separates the two diseases better than any test available on site. The post on pretest probability in diagnosis reminds us that, in a healthy 41-year-old woman, a common stroke is rare, while the exposure shifts the probability toward gas diseases.

The second lesson is about acting under uncertainty. The initial management is the same for both hypotheses, and the doubt between them does not justify delay. The post on diagnostic uncertainty discusses how to decide when the diagnosis is not yet settled. The third lesson is about mechanism: understanding Boyle, alveolar rupture and shunt helps predict pneumothorax and relapse. The post on linking mechanism and symptom develops that habit.

How NEXO helps train this reasoning

To use the case of the day as training, try three habits. Before the first guess, build the timeline from exposure to symptom. With each clue, ask whether it changes management or only the name. After the result, note whether improvement in any symptom made you relax too early.

Three exercises with cases

Draw the timeline. For each case, mark the exposure, the first symptom and the course, and see which hypotheses the interval favors.

Separate management and name. Ask whether the doubt between two hypotheses changes what to do now or only what to write later.

Look for the hidden complication. Write down what other injury the same mechanism could have caused, such as the pneumothorax in this case.

The post on case-based learning shows how cases help fix this habit.

The limits on using the game are described on the NEXO economy page. If you research the teaching of clinical reasoning, the page for researchers explains how to get in touch. Professionals who write or review cases find information under curation and creators, and institutions can learn about the proposal on the partnerships page.

Frequently asked questions

Can arterial gas embolism happen in shallow water?

Yes. The US Navy manual treats as arterial gas embolism the picture of someone who breathed compressed gas, even in a pool, and surfaces unconscious (US Navy Diving Manual, Revision 7).

Does the time to symptom help separate the two diseases?

Yes. Arterial gas embolism usually begins within 10 minutes of surfacing, and decompression sickness has a more spread-out onset (US Navy Diving Manual, Revision 7).

Is oxygen the first aid for both conditions?

Yes. Oxygen at 100 is the first aid and recompression is the definitive treatment (Moon, 2019).

Can the diagnosis be made clinically?

Yes. Imaging often does not show the gas and should not be used to rule out arterial gas embolism (Moon, 2019).

Does screening for patent foramen ovale have a place in follow-up?

Yes. It is indicated for selected high-risk people, with contrast echocardiography or transcranial Doppler (Meng et al., 2026).

Final checklist

• I asked whether the person had breathed compressed gas, even at shallow depth.
• I built the timeline between the ascent and the first symptom.
• I considered arterial gas embolism when neurological symptoms appeared within 10 minutes.
• I looked for spinal signs that suggest neurological decompression sickness.
• I gave oxygen at the highest possible fraction and kept the person lying down.
• I checked blood glucose and repeated the neurological exam.
• I thought about pneumothorax before the chamber.
• I maintained recompression even with normal imaging.
• I adjusted fluids to avoid overload and monitored urine output.
• I planned shunt screening for follow-up, not for the initial assessment.

Want to practice your reasoning with progressive clues? Play the case of the day.

References

1. Banham N, Hawkings P, Gawthrope I. A prospective single-blind randomised clinical trial comparing two treatment tables for the initial management of mild decompression sickness. Diving Hyperb Med. 2022. PMID 35732279.
2. Bonnemaison B, Castagna O, de Maistre S, et al. Chest CT scan for the screening of air anomalies at risk of pulmonary barotrauma for the initial medical assessment of fitness to dive in a military population. Front Physiol. 2022. PMID 36277200.
3. Bresser MF, Wingelaar TT, Van Weering JAF, et al. An observational study ascertaining the prevalence of bullae and blebs in young, healthy adults and its possible implications for scuba diving. Front Physiol. 2024. PMID 38420621.
4. Fakkert RA, Karlas N, Schober P, et al. 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. Crit Care. 2023. PMID 37434172.
5. Meng L, Zhang X, Sun G, et al. Patent Foramen Ovale: Epidemiology, Risk Factors, Pathophysiology, Clinical Features, Diagnosis, and Management. MedComm. 2026. PMID 42707360.
6. Moon RE. Hyperbaric treatment of air or gas embolism: current recommendations. Undersea Hyperb Med. 2019. PMID 31683367.
7. Tetzlaff K, Swenson ER, Bärtsch P. An update on environment-induced pulmonary edema: "When the lungs leak under water and in thin air". Front Physiol. 2022. PMID 36277204.
8. US Navy. U.S. Navy Diving Manual, Revision 7. Naval Sea Systems Command. 2016. Diving publications.
9. Walker SC, Garbino A, Ray K, et al. Oxygen exposures at NASA's Neutral Buoyancy Lab: a 20-year experience. Undersea Hyperb Med. 2018. PMID 30241122.
10. Xu W, Liu W, Huang G, et al. Decompression illness: clinical aspects of 5278 consecutive cases treated in a single hyperbaric unit. PLoS One. 2012. PMID 23185538.