Arterial gas embolisms are caused by the entry of gas into the pulmonary veins or directly into the arteries of the systemic circulation.

• Gas may enter arteries as a result of overexpansion of lungs by decompression barotraumas or result from paradoxical embolus.
• Emboli can travel to any artery, but the most serious consequences occur when they affect the cerebral or coronary circulation.
• Synonym(s): Gas embolism; Air embolism

Incidence

• Predominant age: Young adult
• Predominant sex: Male > Female.

Prevalence
Estimated (based on injury/mortality reports collected by Divers Alert Network) to occur in ~4/100,000 sport divers per year

• Surgery: Recent craniotomy with patient in upright position, cardiothoracic surgery (with cardiopulmonary bypass), hip replacement, cesarean section
• Scuba: Arterial gas embolism is the most serious and rapidly fatal of all scuba diving injuries and is 2nd only to drowning as the leading cause of death associated with sport diving. Arterial gas embolism occurs on ascent from alveolar rupture; time to the manifestation of symptoms is nearly always < 10 minutes.
• History of patent foramen ovale has been associated with a >4-fold increase in decompression illness events and 2-fold more ischemic brain lesions than in divers without this condition.

• Strict adherence to diver safety protocols
• No diving after any dive injury or with any medical condition until evaluated and approved by a physician knowledgeable about diving medicine

• Cerebral air embolism:
  • Air bubbles occlude the brain vasculature.
  • Intracranial pressure (ICP) increases.
  • Unequal distribution of blood in the brain causes hyperemia and ischemia.
  • Small bubbles irritate vascular wall, causing breakdown of blood–brain barrier; small size allows rapid absorption and may cause only brief interruption of cerebral blood flow.
  • Larger air bubbles take longer to absorb (up to several hours) and can cause primary ischemic injury with diffuse brain edema and increased ICP.
• Coronary air embolism is caused by obstruction of coronary arteries by an air bubble.
  • Temporary ischemia of myocardium
  • Labile blood pressure (BP)
  • Arrhythmias
  • Cardiac failure and/or arrest
• Obstruction is possible in any artery. Small emboli in the vessels of skeletal muscles and viscera are well tolerated.

• Pulmonary barotrauma leading to arterial gas embolism also can cause pneumomediastinum, subcutaneous emphysema, pneumopericardium, pneumothorax, and pneumoperitoneum.
• Always consider the possibility of decompression sickness in addition to arterial gas embolism in any scuba diver who has recently completed a dive.

• Cerebral air embolism:
  • Altered mental status
  • Headache
  • Dizziness
  • Paresthesias
  • Visual disturbances
  • Aphasia
  • Minor motor weakness
  • Paralysis
  • Seizures
  • Asymmetric pupils
  • Hemianopia
• Coronary arterial embolism:
  • Chest pain
  • Cardiac arrhythmias
  • Cardiac arrest
• Renal arterial embolism:
  • Hematuria
  • Proteinuria
  • Renal failure
• Mucocutaneous arterial embolism:
  • Cyanotic marbling of the skin
  • Focal area of pallor in the tongue

Rapid onset of new neurologic, cardiac, renal, or mucocutaneous symptoms after completion of a scuba dive or surgery

• Neurologic signs:
  • Altered mental status
  • Aphasia
  • Minor motor weakness
  • Paralysis
  • Seizures
  • Asymmetric pupils
• Cardiac signs:
  • Arrhythmias
  • Arrest
• Renal signs:
  • Hematuria
  • Proteinuria
  • Elevated blood urea nitrogen (BUN)/creatinine
• Mucocutaneous signs:
  • Cyanotic marbling of the skin
  • Focal area of pallor in the tongue

Lab
No specific tests exist for arterial gas embolism.

Initial Labs
Urinalysis and basic metabolic profile (to check for renal involvement)

Imaging

• CXR to rule out pneumothorax
• ECG
• CT scan: Changes often very subtle
• MRI: Sometimes can show increased volume of water in injured tissue (not very reliable)

Decompression sickness

• CPR, if required
• Open airway; prevent aspiration.
• Intubation for somnolent or comatose patient; highest possible concentration of oxygen; eliminates gas in the bubbles by establishing diffusion gradient that favors egress of gas from bubbles
• When air transport is required, helicopter transport should be at an altitude < 1,000 feet, and fixed-wing transfer should be limited to an aircraft that can maintain cabin pressure at 1 atm.

First Line
Oxygen:

• Concentration as high as possible
• Immediate transport to a suitable hyperbaric chamber for recompression

Second Line

• Aspirin
• Adjunctive therapy with glucocorticoids, lidocaine, heparin, or indomethacin: Efficacy unclear

General Measures

• Lifesaving measures must take precedence to sustain life.
• Keep patient recumbent while maintaining patent airway. Place patient in flat supine position (head-down position may aggravate cerebral edema that develops).
• Maintain hydration with IV fluids.
• Hyperbaric oxygen:
  • 1st-line treatment of choice for arterial gas embolism; immediate transport to a suitable hyperbaric chamber for recompression as soon as possible; do not delay because of nonessential procedures.
  • 100% oxygen at pressure above that of the atmosphere at sea level
  • Decreases bubble size
  • Prevents cerebral edema
  • For assistance and advice on locating the nearest treatment chamber in your area, call Divers Alert Network (DAN) at any hour (919) 684-8111. Worldwide contact information available at http://www.diversalertnetwork.org.

IV Fluids
Achieve normovolemia.

None until after treatment

Patient Monitoring
Complete neurologic assessment at 1, 3, 6, and 12 months

Nothing to be consumed until after treatment

• Divers Alert Network: http://www.diversalertnetwork.org
• Diving emergency hotline for medical emergencies only: (919) 684-8111 or (919) 684-4DAN (collect), 365 days a year, 24 h a day
• Medical information for nonemergency questions: (919) 684-2948 M–F (9–5 EST); general information: (800) 446-2671 or (919) 684-2948 M–F (9–5 EST)

Complete to partial resolution with adequate treatment

• Long-term serious neurologic impairments
• Death

• Davis J. Medical Examination of Sport Scuba Divers. 2nd ed. San Antonio, TX: Medical Seminars, 1986.
• Muth CM, Shank ES. Gas embolism. N Engl J Med. 2000;342:476-82 [PMID:10675429]
• Van Hulst RA , Klein J , Lachmann B. Gas embolism: Pathophysiology and treatment. Clin Physiol Funct Imaging. 2003;23:237–246.
• Vann RD , Dovenbarger JA. Reports on decompression illness. Diving fatalities and project dive exploration: The Divers Alert Network Annual Review of Recreational Scuba Driving Injuries and Fatalities. 2002 Data Durham: Divers Alert Network. 2004:1–152.

958.0 Air embolism as an early complication of trauma

302968001 arterial air embolus (disorder)

ALERT

• Any diver who has new symptom(s) or sign(s) after recently completing a self-contained underwater breathing apparatus (SCUBA) dive of any type, to any depth, for any period of time, should be considered for a dive-related injury.

• Anesthesia and/or analgesics alter the symptomatology and may complicate evaluation of the patient’s clinical status. Delayed recovery from general anesthesia may be a clue to cerebral arterial embolism.

Reinier J. van Tonder, MBChB