FOR IMMEDIATE RELEASE
CONTACT: LESLIE CAPO
(504) 568-4806; CELL (504) 452-9166

New Orleans, LA — Dr. Paul Harch, LSUHC Clinical Associate Professor of Emergency Medicine, is the principal investigator of a pilot study to determine the effectiveness of one or two courses of hyperbaric oxygen therapy in treating chronic traumatic brain injury (TBI) and TBI with post traumatic stress disorder (PTSD).  The study grew out of previous experience in treating TBI with hyperbaric oxygen therapy with improvement in symptoms and function.

Thirty participants will be recruited — half will have traumatic brain injury and half will have both traumatic brain injury and post traumatic stress disorder.  The participants will undergo oral, written, and computer tests, ass well as an MRI (if the participant has not had one since injury) and SPECT brain imaging.  Participants will have 40 hyperbaric oxygen therapy treatments and can request up to 40 more if not improved to his/her satisfaction.

Certain conditions preclude participation including pregnancy and increased risk for rare HBOT complications.

Possible benefits include improvement in thinking ability, quality of life, and reduction of PTSD symptoms: however there may be no benefits.

Results will be measured by brain blood flow imaging, written tests for memory and thinking, and questionnaires about quality of life and health.

According to the Centers for Disease Control and Prevention, a traumatic brain injury (TBI) is caused by a blow or jolt to the head or a penetrating head injury that disrupts the normal function of the brain.  The severity of a TBI my range from “mild,” i.e., a brief change in mental status or consciousness to “severe,” i.e., an extended period of unconsciousness or amnesia after the injury.  TBIs contribute to a substantial number of deaths and cases of permanent disability annually.  CDC estimates that at least 5.3 million Americans, about 2% of the U.S. population, currently have a long-term or lifelong need for help to perform activities of daily living as a result of a TBI.

TBI has been called the signature wound of the Wars in Iraq and Afghanistan.  A RAND Corporation study released in April “estimates that about 320,000 service members may have experienced a traumatic brain injury during deployment — the term used to describe a range of injuries from mild concussions to severe penetrating head wounds.  Just 43 percent reported ever being evaluated by a physician for that injury.  One-year estimates of the societal cost associated with treated cases of mild traumantic brain injury range up to $32,000 per case, while estimated for treated moderate to severe cases range from $268,000 to more than $408,000.  Estimates of the total one-year societal cost of the roughly 2,700 cases of traumatic brain injury identified to date  range from $591 million to $910 million.”

A 2005 article in the New England Journal of Medicine, Traumatic Brain Injury in the War Zone, by Susan Okie, MD, says “among surviving soldiers wounded in combat in Iraq and Afghanistan, TBI appears to account for a larger proportion of casualties than it has in other recent U.S. wars.  According to the Joint Theater Trauma Registry, compiled by the U.S. Army Institute of Surgical Research, 22 percent of the wounded soldiers from these conflicts who have passed through the military’s Landstuhl Regional Medical Center in Germany had injuries to the head, face, or neck.  This percentage can serve as a rough estimate of the fraction who have TBI, according to Deborah L. Warden, a neurologist and psychiatrist at Walter Reed Army Medical Center who is the national director of the Defense and Veterans Brain Injury Center (DVBIC).  Warden said the true proportion is probably higher, since some cases of closed brain injury are not diagnosed promptly.”

For more information or to find out if you qualify, call 504-309-4948.

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Department of Defense Brain Injury Rescue and Rehabilitation
SCIENTIFIC BACKGROUND AND OVERVIEW
The Use of Hyperbaric Medicine in Acute Trauma
By
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.