Cerebral Arterial Gas Embolism

7 Interesting Facts of Cerebral Arterial Gas Embolism 

1. In cerebral arterial gas embolism, bubbles of air or other gas embolize and occlude cerebral arteries
2. Most commonly caused by decompression illness or decompression sickness in patients with patent foramen ovale or other left to right shunt
3. Diagnosis is clinical after a provocative decompression event, particularly if patient may have held breath as ambient pressure dropped
4. Neurologic examination is key to physical examination and to diagnosis
5. Symptoms manifest within 15 minutes, and usually within 5 minutes, of decompression event
   • Most common manifestations: stupor or confusion, coma, seizures, unilateral or bilateral motor or sensory deficits, visual disturbances, vertigo, or collapse
   • This profile is indistinguishable from that of severe neurologic decompression sickness, making the symptom timing and characterization of the decompression event vital to diagnosis
6. Chest radiograph is needed to rule out or diagnose pneumothorax, which must be treated before hyperbaric oxygen therapy starts
7. Hyperbaric oxygen therapy is the gold standard treatment 

Pitfalls

• Possibility of this condition may be overlooked in a patient who has completed only a quick, shallow dive
• Failure to detect and treat pneumothorax before starting hyperbaric oxygen therapy can be fatal
• Failure to administer hyperbaric oxygen therapy, especially in a patient who has transient improvement of symptoms (due to redistribution of bubbles), could lead to worse outcomes

• Cerebral arterial gas embolism occurs when 1 or more bubbles of air or other gas enter the arterial circulation of the brain
• Cerebral arterial gas embolism is often associated with decompression illness caused by pulmonary barotrauma from diving, flying, altitude chamber, or treatment in hyperbaric chamber
  • Recent exposure to rapid change in ambient pressure in any of the following scenarios:
    • Diving: intentional or inadvertent breath holding during ascent
      • Especially during rapid ascent, which can be caused by the following:
        • Interruption in or running out of breathing gas
        • Strong currents or waves that lift diver quickly without warning
    • Breath holding during rapid decompression while flying, in altitude chamber, or in hyperbaric chamber
      • Sometimes called explosive decompression, rapid decompression involves quick drop in ambient pressure, such as when an aircraft suddenly loses a door or window at high altitude
• Cerebral gas embolism may also be caused by use of intravascular equipment or present as a perioperative complication of certain procedures, especially those using compressed air

Classification

• Often a result of decompression illness, which is defined as gas bubbles in either arterial or venous circulation 
  • Cerebral arterial gas embolism secondary to decompression illness is the most relevant type for primary care and emergency medicine because diving accidents usually present at local emergency departments or in the field. Etiologies include:
    • Pulmonary barotrauma from diving, flying, altitude chamber, or hyperbaric chamber
    • Entry of venous gas emboli into arterial circulation because of left to right shunt, most often patent foramen ovale
    • Concussive force, such as bomb blasts
  • Gas bubbles in venous circulation is termed decompression sickness
• Iatrogenic types are seen by specialized surgical and critical care teams that are prepared for the possibility of bubble formation 
  • Lung overexpansion (due to barotrauma or volutrauma) during mechanical ventilation
  • Air introduced into circulation by cardiopulmonary bypass, intravascular catheters, or other surgical procedures or devices
  • Peri-operative complication of certain surgeries, especially those using compressed air

Diagnosis

Clinical Presentation

History

• Symptoms are due to acute occlusive process followed by endothelial injury leading to ischemia; local inflammatory process is then triggered resulting in thrombosis, with both vasogenic and cytotoxic edema 
• Symptom timing
  • Symptoms appear within 15 minutes (more than 80% within 5 minutes) of decompression event
• Most common manifestations include the following, although any neurologic manifestation is possible 
  • Stupor or confusion (24%)
  • Coma without seizures (22%), coma with seizures (18%)
  • Unilateral motor deficits, including hemiplegia (14%)
  • Visual disturbances (9%)
  • Vertigo (8%), unilateral sensory deficits (8%), bilateral motor deficits (8%)
  • Collapse (4%)
• Neurologic symptoms and signs may evolve between time of field neurologic examination (performed just after decompression event) and time of presentation at medical facility
  • Manifestations may worsen during this period, but they also may improve, owing to redistribution of arterial bubbles. Improvement can be transient, because bubbles still exist and can move again 

Physical examination

• Neurologic examination
  • Key element of physical examination
  • Any neurologic deficits not known to already exist in the context of ambient pressure changes mandate evaluation
  • Serial measurement of Glasgow Coma Scale score has been used to monitor treatment progress 
• Ophthalmologic examination
  • Careful funduscopic examination may find gas bubbles in retinal arterioles 
• Cardiovascular examination
  • Signs associated with left to right shunt
    • Muffled heart tones, heart murmurs, and neck vein distention
• Lungs
  • Decreased breath sounds
• Skin
  • Crepitus, petechiae, and mottling
• Mucous membranes
  • Discrete area of pallor at base of tongue (Liebermeister’s sign) 

Causes

• Drop in ambient pressure can result in decompression illness
  • Bubbles of inert gas in venous circulation transfer to arterial circulation via patent foramen ovale or other left to right connection
  • Diving, flying, altitude chamber
    • Breath holding when ambient pressure suddenly decreases causes lung overexpansion barotrauma, resulting in alveolar rupture
      • Air or other breathing gases enter pulmonary veins and then left side of heart
      • Once in circulatory system, air emboli go preferentially to cerebral circulation, resulting in cerebral arterial gas embolism, but they also can go anywhere in the body and cause injury
      • Sudden decrease in ambient pressure can result from the following:
        • Rapid ascent during diving
        • Unexpected loss of pressurization in aircraft cabin, hyperbaric chamber, or altitude chamber
• Iatrogenic causes
  • Mechanical ventilation
    • Gas enters pulmonary veins owing to tearing of pulmonary parenchyma, as with diving, flying, or altitude chamber event; overexpansion injury can be either barotrauma or volutrauma
  • Vascular access
    • Air bubbles enter arterial circulation through intra-arterial catheters or enter venous circulation through venous catheters, then transfer to arterial system through patent foramen ovale or other left to right connection; central venous catheter is the most common iatrogenic cause of cerebral gas embolism
    • Air bubbles enter arterial circulation through equipment of extracorporeal cardiopulmonary bypass
  • Other etiologies include lung biopsy, endoscopic retrograde cholangiopancreatography, hemodialysis, mechanical ventilators, and angiography
• Bomb blasts
  • Sudden pressure change from explosion causes lung overexpansion
  • Includes military, terrorism, and industrial explosions

Risk factors and/or associations

Other risk factors/associations

• Cardiac septal defects, such as patent foramen ovale or other potential left to right shunts
  • 25% of adults have patent foramen ovale or pro–patent foramen ovale (foramen ovale is closed but can open if pulmonary pressure increases, for instance, during diving) 
• Chronic or acute pulmonary pathosis, such as the following:
  • Bullae
  • Obstructive disease: increased risk of air embolism because of increased alveolar pressure and shear
    • Chronic obstructive pulmonary disease
    • Asthma (may be associated with increased risk)
  • Smoking-related changes 
  • Pulmonary arteriovenous malformations
    • 70% of these are in patients with hereditary hemorrhagic telangiectasia 
• Mechanical ventilation
  • Chronic pulmonary oxygen toxicity
    • High concentration of oxygen weakens the alveolar-capillary membrane, allowing air to escape into circulation
• Bleomycin-induced pulmonary endothelial cell injury, which exacerbates oxygen toxicity damage 
• Decompression sickness (venous gas emboli) increases the likelihood of cerebral arterial gas embolism in patients with shunts 
• Previous episode of serious decompression sickness increases the likelihood of cerebral arterial gas embolism 

Diagnostic Procedures

Primary diagnostic tools

• Diagnosis is clinical, depending on information in 3 areas, as follows: 
  • Provocative decompression event, particularly if patient may have held breath
    • Rapid ascent during diving
    • Rapid decompression in aircraft, altitude chamber, or hyperbaric chamber
  • Symptom timing
    • Symptoms manifest within 15 minutes, and usually within 5 minutes, of surfacing from a dive
  • Symptom profile
    • Symptoms are indistinguishable from those of neurologic decompression sickness
      • Cerebral arterial gas embolism and decompression sickness also can develop simultaneously, either because of spread of venous bubbles to arterial circulation or because of arterial gas emboli acting as nidus to initiate decompression sickness 
• Chest radiograph is needed to rule out or diagnose pneumothorax, which must be treated before hyperbaric oxygen therapy starts 

Imaging

• Chest radiograph
  • Needed to rule out or diagnose pneumothorax, which must be treated before hyperbaric oxygen therapy starts
  • Subtle signs of non–pneumothorax-related pulmonary barotrauma, such as overdistended alveoli, penetration of air into perivascular interstitium, and interstitial emphysema can be found
    • Presence of such radiographic signs can increase confidence in diagnosis; however, absence of radiographic signs of barotrauma cannot be used to rule out cerebral arterial gas embolism
      • Air can enter pulmonary veins owing to alveolar shearing that is not visible on radiograph; as a result, only 50% of cases of dive-associated cerebral arterial gas embolism show radiographic signs of pulmonary barotrauma 
• CT of chest and head
  • Chest CT is not required before hyperbaric oxygen therapy but will show any non–pneumothorax-related pulmonary barotrauma
  • Head CT is likely to show intracerebral intravascular bubbles, which confirm the diagnosis; however, a negative finding does not rule out the condition
• MRI of head
  • Valuable to identify lesions in brain and to track recovery between sessions of hyperbaric oxygen therapy
  • Perform MRI early in the course of evaluation, as MRI findings may diminish over time 

Functional testing

• Mini–Mental State Examination
  • Assess cognitive status quantitatively by asking patient a series of questions dealing with the following categories, each of which receives a score based on answers:
    • Orientation to time: 0 to 5
    • Orientation to place: 0 to 5
    • Registration: repeating prompted named items: 0 to 3
    • Recall: 0 to 3
    • Repetition: 0 to 1
    • Language: 0 to 2
    • Attention and calculating ability: 0 to 5
    • Complex commands: 0 to 6
  • Category scores are added for a total score of 0 to 30
  • Based on score, degree of impairment is quantified as questionably significant (25-30), mild (20-25), moderate (10-20), or severe (0-10)
• Glasgow Coma Scale
  • Eye opening
    • Spontaneous: 4
    • To speech: 3
    • To pain: 2
    • None: 1
  • Verbal response
    • Oriented: 5
    • Confused conversation: 4
    • Words (inappropriate): 3
    • Sounds (incomprehensible): 2
    • None: 1
  • Best motor response
    • Obey commands: 6
    • Localize pain: 5
    • Flexion to pain
      • Normal: 4
      • Abnormal: 3
    • Extension to pain: 2
    • None: 1
  • Total score ranges from 3 to 15

Differential Diagnosis

Most common

• Neurologic decompression sickness 
  • Gas bubbles in venous circulation
  • Generally takes more than 15 minutes after surfacing from a dive, or after other decompression event, for symptoms appear
  • In contrast, cerebral arterial gas embolism symptoms manifest within 15 minutes after surfacing from a dive or after rapid decompression
  • Very severe neurologic decompression sickness may present so quickly after a dive that it cannot be differentiated from cerebral arterial gas embolism; however, this will not change the treatment
• Middle ear barotrauma 
  • Pressure-induced injury due to air or gas becoming trapped during a change in ambient pressure
  • Patient describes trouble equalizing middle ear pressure during descent (in diving, flying, or altitude chamber), and tympanic membrane damage is visible on otoscopy
  • Can manifest with balance difficulty due to vertigo, which may be suggestive of cerebral arterial gas embolism
  • In contrast, cerebral arterial gas embolism symptoms manifest within 15 minutes after a dive or after rapid decompression
  • Also does not resolve with hyperbaric oxygen therapy, which can be started as a trial if cerebral arterial gas embolism is suspected
• Coincidental, unrelated acute neurologic disorder, such as cerebrovascular accident, intracranial hemorrhage, or spinal hematoma
  • The vast spectrum of cerebral gas embolism presentation could mimic stroke with focal neurologic deficits or even hemorrhage by causing sudden collapse of patient
  • Detectable on imaging (eg, head CT can confirm suspected brain lesion)
  • In contrast, cerebral arterial gas embolism is a diagnosis of exclusion
• Inner ear barotrauma 
  • Pressure-induced injury due to air or gas becoming trapped during a change in ambient pressure
  • Usually occurs during descent. Patient usually describes trouble equalizing middle ear pressure during descent (in diving, flying, or altitude chamber)
  • Condition manifests with tinnitus, conductive hearing loss, pain, and persistent vertigo, but other neurologic symptoms as seen with arterial gas embolism may be seen 
  • A clinical tool accounting for symptom trends, diving history, and otologic testing has been proposed to help distinguish between inner ear barotrauma and decompression sickness 
• Envenomation from marine life, such as blue-ringed octopus
  • Tetrodotoxin produced by the bacteria in salivary glands of octopus is a fast acting toxin that causes paralysis of skeletal muscles while the patient maintains consciousness 
  • Local inflammation is noted at the site of the sting
  • Symptoms of envenomation would not resolve with use of hyperbaric oxygen therapy
• Seafood toxin ingestion
  • In particular, 2 conditions can be mistaken for diving-associated trauma, because most diving takes place in coastal locations, where people visiting to dive also dine on seafood
    • Ciguatera poisoning from eating fish in red tide 
    • Paralytic shellfish poisoning
  • Gastrointestinal symptoms predominate and precede any neurologic symptoms
  • Cerebral arterial gas embolism symptoms develop within 15 minutes after a dive, whereas the median duration to development of symptoms after toxin ingestion is 4 hours 
  • Symptoms of seafood toxin ingestion would not resolve with trial of hyperbaric oxygen therapy
• High-pressure neurologic syndrome
  • Manifests at depth, generally only during very deep dives (120 m or more), with manifestations that can include the following:
    • Headache, tremor, and myoclonus
    • Neuropsychiatric disturbances, similar to cerebral arterial gas embolism
    • EEG changes
  • In contrast, cerebral arterial gas embolism begins after surfacing
  • Differentiate by failure of symptoms to resolve with trial of hyperbaric oxygen therapy
• Carbon monoxide poisoning from contaminated breathing gas during diving 
  • Typically, patient has been diving at a diving facility lacking reputability
  • Very difficult to distinguish from diving-associated cerebral arterial gas embolism in individual patient, but very likely to occur in more than 1 diver on the same dive (ie, if everyone on the dive got a tank with contaminated air, many or all have neurologic symptoms owing to carbon monoxide poisoning, not gas embolism)

Treatment Goals

• Avoid neurologic damage and death
• Achieve complete resolution of condition

Disposition

Admission criteria

Admit all patients with this diagnosis for observation

Criteria for ICU admission

• After initial hyperbaric oxygen therapy, admit all patients to ICU, because any of the following may occur:
  • Need for mechanical ventilation
  • Respiratory distress or other life-threatening respiratory condition as complication of hyperbaric oxygen therapy
  • Persistence of neurologic signs
  • Need for monitoring of intracranial pressure because of concern for delayed cerebral edema
• For patients requiring both critical care and hyperbaric oxygen therapy, administration of hyperbaric oxygen in a multiplace chamber can allow for concurrent administration of critical care in facilities that are prepared to provide those services 

Recommendations for specialist referral

• When presented with a patient with possible symptoms/signs after diving, flying, altitude chamber use, or hyperbaric chamber use, any physician who is not trained in hyperbaric medicine should contact the regional network of diving medicine specialists 
  • In North America, call Divers Alert Network emergency hotline (1-919-684-9111; 24 hours daily) 
• If residual symptoms exist after hyperbaric oxygen therapy, consult with trained hyperbaric physician before allowing patient to fly 

Treatment Options

Stabilize vital signs while arranging transport for definitive treatment (hyperbaric oxygen therapy)

• Give 100% oxygen via nonrebreather mask (10 to 15 L/minute)
  • This should be preferentially initiated as soon as possible by dive boat captains and aircraft pilots 
• Maintain horizontal patient position early in presentation in effort to prevent preferential entry of bubbles into cerebral circulation 
  • But avoid head-down positions, because they can promote cerebral edema 
• Maintain thermal neutrality and avoid hyperthermia (eg, avoid unnecessary sun exposure and excess clothing) 
• Maintain care with parenteral hydration to avoid fluid overload and worsening of cerebral edema 
  • Administer fluids at maintenance rate and titrate to goal urine output of 1 to 2 cc/kg/hour 
• In-water recompression is an extreme last resort measure in settings with very limited resources
  • Harm risk probably outweighs anticipated benefit in symptomatic patients with suspected arterial gas embolism 
  • Contraindications include vomiting, altered level of consciousness, and physical incapacitation that makes return to water unsafe 
  • Procedure involves resubmerging diver in scuba equipment to depth of approximately 9 m of sea water 
  • Requires specifically trained support divers, special equipment, and redundant breathing gas supplies 
  • US military has guidelines and treatment tables for this procedure, which lasts approximately 7 hours using compressed air or 2 to 3 hours using 100% oxygen 

Hyperbaric oxygen therapy

• Hyperbaric oxygen therapy is the gold standard and only effective treatment of cerebral arterial gas embolism associated with diving, flying, altitude chamber, or hyperbaric chamber 
  • This condition always requires hyperbaric oxygen therapy, even when symptoms resolve soon after manifesting
  • For iatrogenic gas embolism occurring during specialized procedures (eg, cardiopulmonary bypass), hyperbaric oxygen therapy also provides definitive treatment; however, with great vessels already accessed and cannulated, surgical team may immediately implement novel treatments, such as the following:
    • Induced, local hypothermia in the brain, achieved by ice around head or with perfusion of cold fluids
    • Retrograde cerebral perfusion
      • Extracorporeal cardiopulmonary bypass circuit is reconnected in a way that reverses blood flow through the brain, thereby bringing the arterial bubble out backward through cerebral arteries
  • For gas embolism from pulmonary volutrauma or barotrauma of mechanical ventilation, hyperbaric oxygen therapy is also appropriate; however, choose a regimen (treatment table) with maximization of air breaks to reduce risk of exacerbating oxygen toxicity
• Hyperbaric oxygen therapy (with table appropriate for cerebral arterial gas embolism) can be given either in monoplace chamber (only the patient is pressurized) or in multiplace chamber (more than 1 patient plus attendants can go inside) 
  • Multiplace drawback: clinicians have limitations on how frequently they can go inside chamber owing to risk of decompression sickness
  • Monoplace drawback: clinicians cannot access patient physically during treatment

Anticoagulation

• Full anticoagulation is not routinely utilized
• Consider enoxaparin or dalteparin for venous thromboembolism prophylaxis, particularly in patients with signs of paraplegia
• Avoid aspirin

Manage increased intracranial pressure in standard fashion

• Invasive intracranial pressure monitoring can be provided if clinician deems it necessary
• Consider lidocaine for neuroprotective effects 
• Avoid corticosteroids 

Drug therapy

• Lidocaine
  • Neuroprotective 
  • Expeditious administration may be used; data are limited
    • Lidocaine Hydrochloride Solution for injection; Adults: 1 mg/kg IV bolus followed by 2 mg/minute infusion until resolution of symptoms. 
      • If lidocaine is used for a prolonged period, maintain a plasma concentration of 2 to 6 mcg/mL (8.5 to 25.6 mmol/L) to prevent toxicity. Terminate IV infusion if toxicity occurs. 
      • Owing to reduced clearance of lidocaine after prolonged infusions, a 50% reduction in the infusion rate may be necessary to avoid toxicity if therapy longer than 24 hours is required.

Nondrug and supportive care

Stabilize vital signs while arranging transport for definitive treatment (hyperbaric oxygen therapy)

For cerebral arterial gas embolism from rapid decompression in aviation setting: descend to lowest possible safe flying altitude

Air evacuation caveats 

• Flight altitude as low as safely possible (less than approximately 150 above pickup location) is preferable
• Maintain cabin pressure of fixed-wing aircraft at 1 atmosphere (sea level [760 mm Hg])
• Use emergency evacuation hyperbaric stretcher when available 

Postrecompression management

• Remain within close proximity of recompression facility for at least 24 hours after therapy
• Avoid flying for at least 3 days after treatment

Procedures

Hyperbaric oxygen therapy 

General explanation

• Exposure to 100% oxygen inside a chamber that is pressurized beyond 1 atmosphere absolute
• Hemoglobin is saturated with oxygen
• Different courses of treatment, known as treatment tables, are available
  • US Navy Table 6A 
  • US Air Force Table 6A 

Indication

• Patient with neurologic symptoms/signs manifesting after a dive, rapid decompression, or ascent to higher altitude
• Patient with sudden, or suddenly worsened, neurologic symptoms/signs associated with pulmonary volutrauma or barotrauma during mechanical ventilation
• Patient with sudden, or suddenly worsened, neurologic symptoms/signs after bubbles are detected (via alarm) in intravascular catheters/lines or cardiopulmonary bypass circuits

Contraindications

• Untreated pneumothorax 

Complications

• Barotraumatic lesions in the following locations: 
  • Middle ear
  • Nasal sinuses
  • Inner ear
  • Lung
  • Teeth
• Oxygen toxicity
  • Central nervous system
  • Lung
• Confinement anxiety 
• Ocular effects
  • Myopia
  • Cataract growth

Invasive intracranial pressure monitoring

General explanation

• There are 3 ways to measure intracranial pressure via invasive placement of monitoring devices
  • Intraventricular catheter
    • Most accurate measurement method
    • Hole is drilled through skull and catheter is placed through brain into lateral ventricle
    • Used for monitoring pressure inside skull as well as removing cerebrospinal fluid if necessary
  • Subdural screw (or bolt)
    • Used when need for pressure monitoring is immediate
    • Hole is drilled through skull and hollow screw is inserted through hole and dura mater
    • Allows pressure recording and cerebrospinal fluid removal from subdural space
  • Epidural sensor
    • Least invasive method
    • Hole is drilled in skull and small sensor is threaded through hole and placed between inner lining of skull and dura mater
    • Cerebrospinal fluid cannot be removed
• May be performed with general or local anesthesia

Indication

• Need for intracranial pressure monitoring
  • Intracranial pressure monitoring has traditionally been used in cases of severe head trauma and acute coma, but routine application has recently been questioned
  • Postoperative monitoring for brain swelling
• Need for sterile access to repeatedly drain cerebrospinal fluid 

Contraindications

• Coagulopathy 
• Incomplete cranial calcification in pediatric patients

Complications

• Bleeding 
• Brain herniation and injury from increased pressure and altered anatomy
• Damage to brain parenchyma from drill or placement of monitor
• Inability to find ventricle and accurately place catheter
• Infection 

Interpretation of results

• Intracranial pressure reference range is 5 to 15 mm Hg 

Comorbidities

• Potential left to right shunt, such as patent foramen ovale
  • Patients often need longer duration of hyperbaric oxygen therapy 
  • After treatment of cerebral arterial gas embolism, screen for patent foramen ovale 
  • 25% of adults have patent foramen ovale or pro–patent foramen ovale (foramen ovale is closed but can open if pulmonary pressure increases, for instance, during diving)
• Pneumothorax
  • Can result from same pulmonary barotrauma event that causes cerebral arterial gas embolism
  • Must be treated before hyperbaric oxygen therapy starts

Monitoring

• Monitoring during recompression therapy
  • Carefully and closely monitor neurologic status with serial Glasgow Coma Scale assessments
  • Deterioration in neurologic status as suggested by Glasgow Coma Scale score requires immediate evaluation by neurologist and may require intracranial pressure monitoring
• Follow-up brain MRI is recommended within 1 week of injury 
• US Navy guidelines on returning to diving after cerebral gas embolism include: 
  • Absence of residual signs and symptoms
  • Normal brain MRI results
  • Normal pulmonary function test results
  • No significant abnormality on noncontrast chest CT result
  • Medical clearance from a pulmonologist and neurologist

Complications

• Delayed cerebral edema, leading to relapse
  • Some degree of relapse may occur in up to 32% of cases, but it is not clear how many such relapses are specifically due to delayed cerebral edema
• Permanent neurologic damage
  • All unfavorable outcomes, including permanent neurologic damage, account for approximately 28% of cases 
• Seizure, coma, or death
  • Second most common direct cause of diving fatality (drowning is number 1). Also is frequently the cause of disability leading to drowning in diving
  • Hyperbaric oxygen therapy given within 6 hours of symptom onset decreases mortality and long-term complications 
  • Poor outcome (ie, death or permanent damage) is more likely when infarct or edema is found on head CT or MRI before hyperbaric oxygen therapy 

Prognosis

• Most patients with cerebral arterial gas embolism from diving, aviation, or iatrogenesis survive, with no major effect on quality of life, when condition is recognized early and patient is referred quickly for hyperbaric oxygen therapy 
• In a systematic review of iatrogenic cerebral gas embolism, 79 out of 249 patients died (32%) and an additional 45 (18%) had at least moderate disability; worse outcomes are typically associated with delays in initiating hyperbaric oxygen 

Screening

At-risk populations

• Persons with history of decompression sickness with cerebral, spinal, vestibulocochlear, or cutaneous manifestations 
  • Some experts suggest that pain-only decompression sickness is not an indication for evaluation of patent foramen ovale 
• Current or earlier history of migraine with aura 
• History of cryptogenic stroke 
• First-degree relative with history of patent foramen ovale or atrial septal defect 
• History of congenital heart disease 

Screening tests

• Consider echocardiography to detect intracardiac shunt, such as patent foramen ovale 
  • Useful to assess for patent foramen ovale or other septal defect
  • Study must include bubble contrast and provocation maneuvers (eg, Valsalva, sniffing) to promote right to left shunting 
  • Patent foramen ovale and other right to left intracardiac shunting increases risk for future episode when present
  • Management of patients identified as having patent foramen ovale include foramen ovale closure and adoption of more conservative diving measures aimed at reducing risk of significant venous bubble formation after diving (eg, use of nitrox, reducing dive times, restricting depths). Some patients may need to discontinue diving 

Prevention

• Advise patients as follows:
  • Dive conservatively: do not violate (or closely approach) limits of decompression profile
  • Avoid breath holding during ascent in diving or during rapid decompression on aircraft, in hyperbaric chamber, or in altitude chamber
  • Frequently train and practice diving skills and altitude procedures
• Adhere to mechanical ventilation protocol to avoid volutrauma and barotrauma
• Properly maintain and operate equipment, such as bubble alarms and other safety devices, for cardiopulmonary bypass and other procedures involving access to blood vessels
• Restrict diving and flying activities if medical status warrants. Entirely seizure-free patients on stable antiepileptic drug therapy for 4 or more years may be allowed to dive to shallow depths if patient and diving buddy both fully understand the risk 

References

1Bennett MH et al: Hyperbaric and diving medicine. In: Jameson J, eds: Harrison’s Principles of Internal Medicine. 20th ed. McGraw Hill; 2018