Department of Defense Brain Injury Rescue and Rehabilitation
The Use of Hyperbaric Medicine in Acute Trauma
Paul G. Harch, M.D.
Clinical Asistant Professor and
Director, Hyperbaric Medicine Fellowship,
Louisiana State University School of Medicine
New Orleans, Louisiana

Hyperbaric oxygen therapy (HBOT) is the use of greater than atmospheric pressure oxygen as a drug to treat basic disease processes and ther diseases(1).  In the simplest terms HBOT is a pharmaceutical or prescription medication similar to the thousands of medications routinely prescribed by physicians everyday throughout the world.    The key differences with HBOT, however, are that it is a drug that treats basic disease processes that are common to every disease, that it acts as a repair drug in these processes, and that it replaces an essential element of life for which there is no substitute, oxygen.  This effectiveness in treating basic common disease processes explains the ability of HBOT to act in a generic beneficial fashion to a multitude of diseases, including and esprecially traumatic injuries to all areas of the body.

HBOT has both acute and chronic drug effects.  HBOT exerts these effects by obeying the Universal Gas Laws, the most important of which is Henry’s Law (2).  Henry’s Law states that the concentration of a gas in solution is proportional to the pressure of that gas interfacing with the solution.  For example, the amount of oxygen dissolved in a glass of water is directly proportional to the amount of oxygen in the air.   Similarly, the amount of oxygen dissolved in our blood is directly proportional to the amount of oxygen we are breathing.  According to Henry’s Law, there is a very small amount of oxygen dissolved in the liquid portion of the blood when breathing air (21% oxygen) at sealevel.  The remainder and majority of oxygen is bound to hemoglobin in the red blood cells giving a 98@ saturation of hemoglobin.    As we increase the amount of oxygen in inspired air by applying a nasal cannula or facemask of pure oxygen the final 2% of hemoglobin is quickly bound by oxygen.  All of the remaining available oxygen interfaces with and is dissolved in the liquid portion of the blood.  Once we reach 1.5 liters/minute of supplemental  oxygen by a tight fitting aviator’s mask or non-rebreather mask we have reached the maximum amount of oxygen that can be dissolved in blood by natural means.  However, this is not the absolute limit.  By placing a patient in an enclosed chamber,  increasing the pressure above ambient pressure, and giving the patient pure oxygen we can cause an increase in dissolved oxygen in blood in direct proportion to the pressure increase.

At the point of three atmospheres absolute of pure oxygen (3 ATA), just slightly more than the amount the U.S. Navy has used for 50 years in the treatment of divers with decompression sickness, we can dissolve enough oxygen in the plasma to render red blood cells useless.  Under these conditions as blood passes through the tiniest blood vessels tissue cells will extract all of the dissolved oxygen in the blood without touching the oxygen bound to hemoglobin.  This amount of dissolved oxygen alone can exceed the amount necessary for the tissue to sustain life.  In other words, you don’t need red blood cells for life at 3 ATA of 100% oxygen.   This physical phenomenon was proven in a famous experiment in 1960 and published in the first edition of the Journal of Cardiovascular Surgery by Dr. Boerema of the Netherlands (3).  Dr. Boerema anesthetized pigs, removed nearly all of their blood, and replaced it with salt water while he compressed them to 3 ATA.  At 3 ATA in a hyperbaric chamber pigs with essentially no blood were completely alive and well.  This phenomenon has been proven effective in other experiments and is the basis for clinical use in extreme blood loss anemia (4).  The best examples are Jehovah’s Witness patients who have lost massive amounts of blood and because of a religous proscription are unable to receive blood transfusions.  These patients are kept alive over weeks with repetitive HBOT until their blood system is able to naturally produce enough blood to sustain life.  This ability to maintain life without blood has obvious potential to battlefield casualties awaiting transfusion.

As a result of Henry’s Law HBOT is able to exert a variety of drug effects on acute pathophysiologic processes.  These have been well documented over the past 50 years and include reduction of hypoxia (5,6), inhibition of reperfusion injury (7), reduction of edema (8), blunting of systemic inflammatory responses (9), and a multitude of others (10).  In addition, repetitive HBOT in wound models acts as a DNA stimulating drug to effect tissue growth (11,12).  HBOT has been shown to interact with the DNA of cells in damaged areas to begin the production of repair hormones, proteins and cell surface receptors that are stimulated by the repair hormones (13,14).  The resultant repair processes include replication of the cells responsible for tissue strength (fibroblasts) (15), new blood vessel growth (16,17), bone healing and strengthening (18), and new skin growth.

To best understand the effectiveness and potential of HBOT one must understand basic disease processes, commonly referred to as pathophysiolocic processes.  Every insult or injury to living organisms, particularly human beings, is distinct and different, and can be characterized by the type of force, energy, or peculiar nature of that insult.  For example, a blast force is different from a blunt force, an electrical injury, a toxic injury, a biological injury, infectious injury, thermal injury, nuclear injury, gunshot wound, stab wound , burn, or even a surgical wound.  Regardless of the exact nature and idiosyncratic character of the injury, however, every acute injury has a common secondary injury called the inflammatory process (20).  This secondary injury in fact causes more damage than the primary injury.  Moreover, it is a universal process common to every human being regardless of race, color, creed, size, gender or genetics.  The beauty of hyperbaric oxygen therapy is its ability to powerfully impact the inflammatory reaction and its component processes like no other drug in the history of medicine.

The inflammatory process begins with tissue injury.  The injury can be as innocuous as apposition of tissues that normally do not interface against one another, such as a spinal bony compression of a nerve root due to a degenerative disk.  Most often, however, tissue injury results from much larger forces such as the type seen in military conflict.  Once tissue is disrupted, proteins, fat, other molecules, and disrupted tissue is exposed to the circulation.  In addition, blood vessels are damaged both directly by mechanical forces and indirectly by tissue fragments that interact with the vessel walls.  The net effect is bleeding from broken blood vessels and dilation of the unbroken blood vessels.  As the vessels dilate, blood pressure forces the liquid portion of the blood out of the vessels.  The extravasated fluid, now referred to as edema, exerts its own pressure that collapses blood vessels, leading to a reduction of blood flow.  This compounds the reduction in blood flow already caused by disrupted blood vessels and bleeding.  In addition, white blood cells in the the circulation are attracted to the damaged tissue by molecules released from the damaged tissue.  The white blood cells traverse the blood vessel walls in a process called emigration (21) and disgorge themselves of their digestive enzymes.  These enzymes cause further tissue damage in an attempt to clean up the primary damage, but also cause constriction of blood vessels to limit further bleeding and leakage of fluid.




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HBOT also has beneficial effects on vasospasm and cellular reperfusion injury.  Multiple studies have shown that HBOT reduces cerebral edema and decreases intracranial pressure (ICP).   A summary of the HBOT/cerebral edema studies in animals is that HBOT has two differenct effects: one reducing brain edema (injured brain), and another producing brain edema (normal brain).  This toxic effect on normal brain causes a breakdown in the protective vasoconstriction of arterioles, resulting in a rapid rise in brain blood flow and deterioration in EEG.

Rockswold in 1992 reported the most exhaustive, rigorous, and important study to date in acute TBI (traumatic brain injury) in an attempt to refute or affirm all of the above animal and human data.  Conducted from 1983 to 1989 the study enrolled 168 patients with GCS or 9 or less in a RPCT design and stratified the patients by age and GCS.  Patients were treated at 1.5 ATA/60 every 8 hours for a maximum of two weeks immediately post TBI or until awake or deceased during these two weeks.  The average patient entered treatment 26 hours post TBI and received 21 treatments.  Overall mortality was significantly reduced 50% in the HBOT group and as high as 56% and 60% in the elevated ICP and GCS 4-6 subgroups.

This reduction in mortality has never been equaled by any therapy in the medical armamentarium except possibly the ambulance, or in the case of the military, the helicopter.  Adding HBOT to helicopter evacuation of casualties should further decrease morbidity and mortality of injured soldiers.  This is the foundation of the DoD-BIRR Project.


Harch, Paul, M.D., “FEB Scientific Background and Overview,” 2005 (81 scientific references)

Harch, Paul, M.D., “Evidence for Use of Hyperbaric Oxygen Therapy for Acute Traumatic Brain Injury,” 2001