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Diving gas embolism results from intravascular introduction of gas bubbles, most commonly due to rapid ascent while holding breath, leading to pulmonary overinflation and vascular gas entry. Etiologic factors include inadequate decompression, breath-holding, equipment malfunction, and exposure to high-pressure gas mixtures. Risk increases with deep or prolonged dives, rapid ascents, preexisting pulmonary disease, and age-related pulmonary changes. The pathophysiology involves mechanical obstruction of blood vessels, ischemia, and endothelial injury, with secondary inflammatory responses. The clinical presentation varies from acute neurological deficits, chest pain, dyspnea, and syncope to cardiovascular collapse. Diagnosis relies on history of recent dive, clinical findings, and imaging such as computed tomography or echocardiography demonstrating intravascular gas. Management centers on immediate administration of 100% oxygen, stabilization of the airway and circulation, and hyperbaric oxygen therapy to reduce bubble size and tissue ischemia. Complications include persistent neurological deficits, pulmonary injury, and cardiac dysfunction. Prognosis depends on rapid recognition, timely hyperbaric therapy, and the severity of embolic events, with early intervention improving functional outcomes. This activity for healthcare professionals is designed to strengthen learners' competence in evaluating and managing diving gas embolism. Participants will advance their mastery of the condition's etiology, risk factors, pathophysiology, clinical presentation, and evidence-based diagnostic and therapeutic approaches. Improved skills will equip clinicians to collaborate with interprofessional teams providing care for at-risk individuals. Objectives: Identify the clinical and diagnostic features of diving gas embolism. Implement personalized, evidence-based strategies for managing diving gas embolism and mitigating its potential sequelae. Improve patient awareness of safe diving behaviors, recognition of overexpansion injuries, and immediate response to suspected arterial gas embolism. Collaborate with the interprofessional team to educate, treat, and monitor patients at risk of diving gas embolism to optimize outcomes. Access free multiple choice questions on this topic.

Diving with an underwater breathing apparatus exposes the diver to compressed gas at pressures exceeding normal surface levels. Seawater is denser than air, such that 1 atm of pressure corresponds to 33 fsw. Consequently, ambient pressure on a diver doubles within the first 33 feet of descent. During a dive, the diver is subject to Boyle’s Law, which states that pressure and volume are inversely proportional. Volume increases proportionally as pressure decreases. A diver ascending from 33 fsw while holding a breath would theoretically double lung volume, a condition incompatible with normal pulmonary anatomy. Factors such as acute exacerbation of reactive airway disease, preexisting anatomical anomalies (eg, bullae or blebs), or breath-holding can trap air within the lungs.[1] Subsequent ascent of as little as 1 m (approximately 3 ft) can generate sufficient overpressurization to rupture alveoli and introduce gas into surrounding tissues or the vasculature.[2][3][4] This condition, known as pulmonary overinflation syndrome, may result in 1 or more overexpansion injuries, including pneumomediastinum, pneumothorax, subcutaneous emphysema, or arterial gas embolism (AGE).

AGE is rare, occurring in diving and other forms of dysbarism, including unexpected rapid depressurization in commercial or military aircraft or spacecraft. More frequently, gas may be arterialized during medical procedures such as cardiopulmonary resuscitation, central or peripheral venous access, surgical interventions, and needle biopsies.[5] In theory, gas introduction is possible at any time the vasculature is accessed. Small volumes of gas, typically less than 30 cc, entering the venous system are usually filtered by the lungs and remain asymptomatic. However, gas introduced directly into the arterial system can form emboli in distal arterioles, frequently causing end-organ damage.[6] Arterialization of gas in the brain typically results in stroke-like symptoms or unconsciousness. Smaller gas volumes may also be arterialized via a shunt, such as a patent foramen ovale (PFO) or intrapulmonary shunt. Exact rates in the general population are unknown, but PFOs are documented in approximately 26% to 28% of adults. Accounting for all intrapulmonary, intracardiac, and physiological right-to-left shunts, such shunting may occur in up to 1/3 of adults.

Decompression illness (DCI) encompasses all decompression-related maladies experienced by humans. The condition encompasses 2 primary categories: decompression sickness (DCS), a constellation of conditions resulting from bubble formation due to excess dissolved gas, and overexpansion injuries, including AGE, which result from gas expanding directly under Boyle’s Law as ambient pressure decreases. Diving-related injuries are rare, with an overall incidence ranging from 1 to 3 per 10,000 dives. AGE is at least an order of magnitude less common, with an estimated incidence of fewer than 1 per 100,000 dives. Iatrogenic gas embolism occurs when gas is introduced into the arterial system during a medical procedure.[7] While it is also treated with recompression, iatrogenic embolism is typically unrelated to ambient pressure changes and usually does not cause pulmonary injury. In rare circumstances, overexpansion injuries may result from blast overpressurization or rapid decompression in aircraft or spacecraft.

Gas entering the arterial system can reach the cerebral vasculature and cause a typically transient embolism, analogous to a thromboembolism but of shorter duration.[8][9] Endothelial injury follows, leading to upregulation of inflammatory mediators and stroke-like symptoms. Multiple embolic regions can form since gas is usually distributed as multiple bubbles of varying sizes, producing crossed neurological deficits. When right-to-left pulmonary or intracardiac shunts exist, venous gas that would otherwise be asymptomatic may become arterialized and result in cerebral AGE. Loss of consciousness occurring within 10 minutes after surfacing from a dive or following an invasive procedure should raise immediate suspicion for gas embolism until it can be definitively excluded, regardless of whether the event is transient. Earlier theories proposed that gas remained lodged in vessels until recompression caused bubble shrinkage. Current evidence indicates that gas emboli are almost always transient, with injury resulting from endothelial damage and secondary inflammatory responses. Hyperbaric oxygen therapy (HBOT) downregulates this inflammation and directly resolves edema via arterial vasoconstriction in precapillary beds induced by hyperoxia. Definitive treatment for AGE requires hyperbaric therapy.[10] Normobaric oxygen, delivered by high-flow nonrebreather or demand mask, is the initial treatment for all DCI cases, including AGE, but is not definitive. Discontinuing oxygen administration before recompression often leads to symptom relapse. Recompression is a Class I recommendation and remains the gold standard of care. Field and hospital care should include oxygen at 15 L/min via nonrebreather or demand mask until recompression is available. Extended oxygen therapy prior to recompression is safe for at least the first 12 hours. Prolonged therapy may continue during transport, with hyperbaric physician consultation recommended, especially for patients traveling over unpressurized altitudes.

Patient history is typically consistent with exposure to decreased ambient pressure, such as surfacing from a dive or rapid decompression of an aircraft or spacecraft. Rarely, gas embolism may result from blast overpressure near an explosion. Divers may report rapid or panicked ascent, loss of buoyancy control, or breath-holding during ascent. Iatrogenic emboli may occur during procedures that access the vasculature, including placement or withdrawal of central lines, cardiac catheterization, vascular interventions, robotic hysterectomy and other gynecological procedures, and needle biopsy of pulmonary masses.[11] Cerebral AGE has also been documented from peripheral intravenous placement during cardiopulmonary resuscitation, with intravascular gas confirmed on computed tomography (CT) imaging. Uncommon mechanisms include hydrogen peroxide ingestion, direct inhalation of helium from a pressurized tank, and orogenital exposure during pregnancy. Most patients present with unconsciousness within 10 minutes of gas introduction or surfacing from a dive associated with embolism, often accompanied by crossed neurological deficits. Neurological findings do not consistently correspond to a single lesion, a feature that should raise clinical suspicion for cerebral AGE. Crossed signs, including motor weakness or paralysis, are common. A thorough cerebellar examination should be performed as part of the complete neurological assessment, as subtle deficits may otherwise be missed. Posterior signs and symptoms are frequently present but often overlooked in both cerebral AGE and neurological DCI.

The diagnosis of cerebral AGE is primarily clinical, based on a history suggestive of gas entry into the vasculature (eg, central venous line manipulation or surfacing from a dive) and neurological findings or syncope occurring within 10 minutes of the suspected insult. Radiographic evaluation is not mandatory when history and examination findings are definitive. Rapid acquisition of chest radiography may be performed to evaluate for pneumothorax or other injuries requiring attention prior to recompression. Noncontrast CT of the head may also be indicated if the etiology is uncertain. Finger-stick blood glucose testing is recommended, as crossed neurological deficits may result from hypoglycemia as well as AGE, and testing does not delay recompression therapy. Divers remain susceptible to the same conditions as nondivers and should be evaluated accordingly. The differential diagnosis should remain broad. Recompression should never be delayed when the clinical diagnosis supports AGE.[12] A normal head CT does not exclude cerebral AGE, as most gas emboli are transient. Visualization of gas on CT is pathognomonic and constitutes an immediate indication for recompression. Such findings typically indicate a massive gas load, which is associated with increased morbidity and mortality. Large gas loads often produce multiple emboli without a distinct pattern on CT or magnetic resonance imaging (MRI). While noncontrast-enhanced CT may occasionally demonstrate gas, the absence of radiographic findings does not rule out embolism. MRI may appear normal or demonstrate extensive areas of infarction with associated edema. Although no current theory fully explains this discrepancy, evidence from Air Force high-altitude chamber research demonstrates this phenomenon consistently in confirmed cases of cerebral AGE.[13]

Treatment of cerebral gas embolism consists of immediate recompression on 100% oxygen. First-aid measures include placing the patient on high-flow oxygen via a nonrebreather or demand mask until recompression is available. Patients who are unstable or have a Glasgow Coma Scale (GCS) score below 8 usually require intubation for ventilatory support when the hyperbaric chamber can accommodate a ventilator. Early consultation with a hyperbaric physician is essential, particularly for individuals who are critical or require intubation.[14] Fluid resuscitation should utilize nondextrose-containing solutions. Although early animal studies suggested a benefit of intravenous lidocaine, subsequent research has failed to confirm efficacy. No evidence supports aspirin use for gas embolism. Multiple hyperbaric treatments (3 to 5 or more) may be required before substantial resolution is observed. However, immediate improvement often occurs with recompression. Delays in treatment reduce the likelihood of prompt recovery. In sporadic cases, endovascular procedures may induce both gas embolism and thromboembolism from vessel wall plaque, producing a mixed clinical picture. No established guidelines exist for treatment in these instances, and some evidence suggests hyperbaric therapy may worsen outcomes in acute ischemic stroke. Treatment decisions should be made by the hyperbaric physician, with neurology consultation as appropriate. Normobaric oxygen is insufficient for definitive treatment, even if initially effective at 1 atm, as symptom recurrence is common without recompression. Prehospital treatment of divers with suspected gas embolism should include administration of high-flow oxygen and rapid transport to an emergency department capable of evaluating and differentiating serious neurological injuries. The head-down and lateral decubitus positions are no longer recommended during transport.

In sporadic cases, endovascular procedures may induce both gas embolism and thromboembolism from vessel wall plaque, producing a mixed clinical picture. No established guidelines exist for treatment in these instances, and some evidence suggests hyperbaric therapy may worsen outcomes in acute ischemic stroke. Treatment decisions should be made by the hyperbaric physician, with neurology consultation as appropriate. Normobaric oxygen is insufficient for definitive treatment, even if initially effective at 1 atm, as symptom recurrence is common without recompression. Prehospital treatment of divers with suspected gas embolism should include administration of high-flow oxygen and rapid transport to an emergency department capable of evaluating and differentiating serious neurological injuries. The head-down and lateral decubitus positions are no longer recommended during transport. The generally accepted HBOT protocol is the U.S. Navy Treatment Table 6, with conversion to Table 6A and a deep excursion to 165 fsw if no improvement occurs during the first 10 minutes at 60 fsw. Treatment is most efficacious when initiated within the first 2 hours of symptom onset. Most centers consider Table 6 outside this window, often extended or repeated consecutively, to be adequate. This protocol is based on the principle that gas has typically traversed the vasculature, eliminating the need for a deep “bubble-crushing” excursion to 165 fsw and thereby reducing risk to both the patient and chamber personnel. Use of a nitrogen-based mixture is avoided, minimizing the theoretical risk of additional bubble growth. Extended Table 6 treatments may also benefit patients when the clinical distinction between AGE and cerebral DCS is unclear. Patients with iatrogenic AGE who have not inhaled compressed gas generally do not require compression to 165 fsw, as a minimal gas load requires elimination.

The most likely nondiving conditions to mimic cerebral AGE are acute hypoglycemia and ischemic or hemorrhagic stroke. Cerebral AGE is a clinical diagnosis, typically presenting with loss of consciousness, altered mental status, and crossed neurological deficits. However, an acute hemorrhagic stroke may rarely present after a dive. Physicians uncertain of the diagnosis should consider a STAT noncontrast-enhanced CT of the head if hemorrhagic cerebrovascular accident is suspected, but imaging should not delay recompression by more than a few minutes. Hypoglycemia can produce similar neurological deficits and is more commonly encountered. Therefore, rapid assessment of blood glucose is recommended, as it does not delay recompression. Additional advanced imaging, including MRI, is generally unnecessary unless the neurological deficit is attributable to a single-vessel lesion. Rare neurological disorders could mimic gas embolism but are unlikely to manifest immediately following a dive and may typically be deferred until a trial of recompression has been performed. Postdive venous gas emboli (VGE) are commonly detected in divers. VGE passing into the arterial circulation via a right-to-left shunt can occlude arterial blood flow to tissues, producing ischemia-related symptoms, including severe neurological deficits, shortly after surfacing. Arterialized VGE are thought to produce a symptom progression distinct from AGE, resulting from pulmonary overinflation.[15] Nevertheless, initial differentiation between the 2 can be challenging. Treatment protocols for both conditions are similar. Therefore, early recompression takes precedence over definitive diagnosis. Accurate identification becomes important for follow-up evaluation and assessment of fitness to dive. For example, a diver experiencing severe neurological DCS after proper decompression from an uneventful dive may be considered for PFO testing. In contrast, a diver presenting with unexplained AGE may require radiographic evaluation of the lungs to identify potential underlying pathology.

The prognosis of cerebral AGE directly correlates with the interval to recompression. Most patients experience favorable outcomes when recompression occurs within the first 2 hours. Recompression within 6 hours frequently results in symptom improvement and, in some cases, full resolution. Poorer outcomes are associated with delays exceeding 6 to 8 hours, usually resulting from late diagnosis or delayed transfer to a hyperbaric chamber.

Complications of HBOT are uncommon and include pneumothorax, oxygen-induced seizure, and barotrauma. Pneumothorax resulting from overexpansion injury should be treated with tube thoracostomy before diving or adjusting chamber depth, as expansion during ascent is likely. Otic barotrauma may be prevented through the education of conscious divers. Unconscious or intubated divers may develop hemotympanum during recompression, or a myringotomy may be performed prior to treatment. Recompression should never be delayed for a myringotomy if specialist intervention is required. Hyperbaric physicians should be proficient in the procedure, but recompression should commence even if specialized equipment is not immediately available. Oxygen-induced seizures during treatment are not indications to discontinue therapy. Seizures should be allowed to resolve before any adjustment of chamber depth to avoid additional injury during ascent.

Organized diving training includes instruction on preventing pulmonary overinflation by avoiding breath-holding, controlling ascent rate and buoyancy, and carefully monitoring breathing gas consumption to prevent depletion underwater. Following resolution of the acute injury, the physician should review the dive history with the patient to identify potential precipitating events, such as loss of buoyancy control, abrupt depth changes, or rapid or panicked ascent. If a cause is identified, preventive strategies should be discussed before the diver returns to diving. Decisions regarding return to diving should consider the etiology of the original event and the presence of any residual neurological or pulmonary deficits.

Recompression of patients with AGE constitutes a medical emergency, with outcomes directly dependent on time to treatment. Most patients who undergo recompression within 2 hours achieve favorable outcomes, whereas recovery rates decline markedly when treatment is delayed 6 hours or longer. Symptom reversal has been documented with recompression up to 24 hours after onset, establishing a generally accepted treatment window based on expert consensus. Recompression up to 48 hours after embolization in circumstances that are exceptional or justified on compassionate grounds has demonstrated limited success. Return-to-diving recommendations following AGE must be tailored to each diver’s unique clinical situation and recovery. Divers who experience the condition without an identifiable precipitating event, such as loss of buoyancy control, abrupt depth change, or rapid or panicked ascent, should undergo radiographic evaluation for structural lung abnormalities. The diver should be counseled against returning to diving and referred to a pulmonologist if findings such as bullae, blebs, or cysts are present. Counseling on preventive measures should be provided, and return to diving may be considered when a precipitating event can be reasonably identified and the diver has no residual symptoms. The period required for pulmonary barotrauma recovery before returning to diving is variable and patient-specific.[16] The Association of Diving Contractors International Consensus Standards 6.3 Edition (4 May 2020) specifies 3 months following resolution of pulmonary barotrauma. The U.S. Navy previously recommended a 30-day interval after complete symptomatic improvement. Revision 7 of the U.S. Navy Diving Manual now generally stipulates referral to an Undersea Medical Officer for clearance before returning to diving. Divers with residual symptoms should not resume diving until full resolution.

Early communication with a hyperbaric specialist is essential to ensure timely treatment of AGE. Although stroke-like symptoms and chest pain can occur with overexpansion injuries, the diagnosis of cerebral AGE is primarily clinical. Consultation with specialists in cardiac or neurological emergencies may be appropriate, but should follow the initiation of recompression unless the presentation is atypical for AGE. Inpatient services should be notified, as patients typically require observation and multiple hyperbaric treatments. Ideally, the evaluating physician should be fellowship-trained in undersea and hyperbaric medicine and possess emergency medicine training, facilitating comprehensive evaluation, stabilization, management, and disposition. Successful management of severe diving-related injuries requires coordinated care across the spectrum: knowledgeable emergency medicine services personnel, initial evaluation at an emergency department, transfer to a hyperbaric-capable center, consultation with a hyperbaric physician experienced in diving medicine, preparation and support by hyperbaric nurses, supervision by diving technicians, and care within the chamber by trained hyperbaric tenders. Dedicated safety and operations personnel are essential to ensure proper chamber function and fire safety during treatment.