Air or gas embolism occurs when gas bubbles enter arteries, veins and/or capillaries. This results in reduced blood flow and poor oxygen delivery to the areas supplied by the affected circulation. If not fatal, gas embolism can result in severe, long-standing and irreversible physical and emotional disabilities. There can be weakness or paralysis in the limbs; vision can be impaired or absent; brain, heart, lung and other organ damage may occur. Limited use of remaining functions can be sufficiently severe that total disability results. Those who do not die may be limited to walking with canes, crutches or walkers. Those more severely disabled may be wheelchair confined or bedridden. These outcomes may be permanent and may severely impact quality of life. Maximal medical treatment of the condition is necessary to ensure the best possible degree of recovery from this potentially disastrous problem.

Hyperbaric oxygen has been shown to reduce the size of bubbles obstructing circulation. The increased pressure in the hyperbaric chamber reduces bubble size and drives the remaining gas into physical solution, while the high oxygen pressure washes out inert gas from the bubble. When bubbles are smaller or resolved, blood flow resumes. Poorly oxygenated tissues then receive higher levels of oxygen delivery. Another problem in gas embolism is that vessels obstructed by bubbles may leak fluid into surrounding tissues, resulting in swelling. Such swelling can further reduce tissue blood flow. When flow is restored, the local swelling will subside with resultant improvement in circulation and oxygen supply. Finally, the high levels of oxygen provided in the hyperbaric chamber have the potential to immediately restore cellular oxygen levels while blood flow impairment and tissue swelling are being corrected.

Hyperbaric oxygen treatment is the primary treatment for gas embolism and a major review of reported cases clearly indicates superior outcomes with its use compared to non-recompression treatment.


  1. Mushkat Y, Luxman D, Nachum Z, David MP, Melamed Y. Gas embolism complicating obstetric or gynecologic procedures. Case reports and review of the literature. European Journal of Obstetrics, Gynecology, & Reproductive Biology 1995;63:97-103.
  2. Boussuges A, Blanc P, Molenat F, Bergmann E, Sainty JM. Prognosis in iatrogenic gas embolism. Minerva Medica 1995;86:453-457.
  3. Weiss LD, Van Meter KW. The applications of hyperbaric oxygen therapy in emergency medicine. American Journal of Emergency Medicine 1992;10:558-568.
  4. Kindwall EP. Uses of hyperbaric oxygen therapy in the 1990s. Cleveland Clinic Journal of Medicine. 1992;59:517-528.
  5. Dutka AJ. Air or gas embolism. In: Hyperbaric Oxygen Therapy: A Critical Review. Camporesi EM, Barker AC, eds. Bethesda, MD, Undersea and Hyperbaric Medical Society, 1991:1-10.

Selected references on Gas Embolism:

  • Anon: U.S. Navy Diving Manual, Volume 1 (Air Diving) 1993, Revision 3:8-18--8-20. Best Publishing Co., Flagstaff, Arizona.
    The authoritative text of the
    United States military government. It notes, among other things, that "… unless treated promptly and properly by recompression (hyperbaric oxygen therapy), arterial gas embolism is likely to result in death or permanent brain damage".
  • Anon: NOAA Diving Manual, Diving for Science and Technology 1991, 20-9--20-13.
    The authoritative text of the
    United States civilian government. It states, among other things, that "Prompt recompression (hyperbaric oxygen therapy) is the only treatment for gas embolism".
  • Waite CL, Mazzone WF, Greenwood, ME, et al: Cerebral air embolism, I. Basic studies. Submarine Medical Research Laboratory, U.S. Naval Submarine Medical Center Report No. 493:1-14.
    Historically significant publication from the U.S. Navy Bureau of Medicine and Surgery. It compares hyperbaric treatment to no hyperbaric treatment in an open-brain model of gas embolism. Dogs not treated hyperbarically "all died or were left with severe residual neurological defects". All of the hyperbarically-treated animals made a complete recovery, with one exception. This research paved the way for the modern hyperbaric treatment protocols for gas embolism.
  • Moon RE: Gas embolism. Handbook on Hyperbaric Medicine, Eds. Oriani G, Marroni A, Wattel F. Springer, Italy 1966:229-248.
    Comprehensive review article.
  • Helps SC, Gorman DF: Air embolism of the brain in rabbits pretreated with mechlorethamine. Stroke 1991;22:351-354.
    The third in a series of articles published in STROKE by these authors. They have demonstrated a more complex pathophysiology than that previously appreciated. Cerebral arterial embolization results in flow deficit, ischemia, followed by a reperfusion-like injury component in many cases. Such ischemia-reperfusion complications require the presence of leukocytes. Hyperbaric oxygen is necessary to support areas of critical flow impairment. Hyperbaric oxygen will also serve to antagonize leukocyte-mediate ishemic-reperfusion injury (see #5, Acute Traumatic Peripheral Ischemia, Article #9, Zamboni, et al).
  • Reasoner DK, Dexter F, Hindman BJ, et al: Somastosensory evoked potentials correlate with neurological outcome in rabbits undergoing cerebral air embolism. Stroke 1996;27(10):1859-1864.
    Validation of the Helps and Gorman’s (above) model of using evoked potentials to correlate neurological outcome in gas embolism.
  • Kol S, Ammar R, Weisz G, et al: Hyperbaric oxygenation for arterial air embolism during cardiopulmonary bypass. Ann Thorac Surg 1993;55:401-403.
    Representative paper addressing one of the many iatrogenic etiologies of gas embolism. It reports the morbidity and mortality associated with this complication when HBO therapy is not utilized. It further described the importance of early hyperbaric referral and treatment.
  • Bitterman H, Melamed Y: Delayed hyperbaric treatment of cerebral air embolism. Isr J Med Sci 1993;29(1):22-26.
    A report of the efficacy of HBO therapy in reversal of latent coma, hemiplegia, and hemiparesis.
  • Leitch DR, Greenbaum LJ, Hallenbeck: Cerebral arterial air embolism: II. Effect of pressure and time on cortical evoked potential recovery. Undersea Biomed Res 1984;11(3):237-248.
    Compares treatment protocols in a "severe" model of gas embolism " … no treatment surpassed oxygen at 2.8 bar" (hyperbaric oxygen therapy).
  • Leitch DR, Greenbaum, LJ, Hallenbeck: Cerebral arterial air embolism: IV. Failure to recover with treatment, and secondary deterioration. Undersea Biomed Res 1984;11(3):265-274.
    Comparison of treatment protocols in a "severe" model of gas embolism. Hyperbaric doses of air and oxygen were compared to normobaric (non-hyperbaric) air. In extrapolating this model to the clinical arena "…the majority of patients with severe arterial gas embolism will achieve maximum benefit from compression to 2.8 bar while breathing oxygen", i.e.,hyperbaric oxygen therapy.
  • McDermott JJ, Dutka AJ, Koller WA, et al: Effects of an increased P02 during recompression therapy for the treatment of experimental cerebral arterial gas embolism. Undersea Biomed Res 1992;19(6):403-413.
    Highly significant outcome improvement when two standard hyperbaric treatment protocols were compared to non-hyperbaric air.
  • Kearns PJ, Haulk AA, McDonald TW: Homonymous hemianopia due to cerebral air embolism from central venous catheters. The Western Journal of Medicine Case Reports 1984;140(4):615-617.
    Reports the sustained neurological compromise (infarcts via C.T. scan) in patients with gas embolism not treated hyperbarically.