The Future of TBI: Hyperbaric Oxygen as a Primary Therapeutic Approach


Introduction

The human body breathes in and out an average of 10–16 times per minute. The air we breathe contains 21% oxygen, 78% nitrogen, and 1% carbon dioxide and other gases. For an average adult body, the volume of each breath is between 400 and 600 mL. This equals roughly 6–8 L of air per minute. Taking 21% of 6 L equals about 1.3 L of oxygen every sixty seconds. The standard pressure of that air is 1 atm equivalent, or 1 ata, which is equal to roughly 14.5 psi, or 760.00 mm Hg on a barometer. The density of air at sea level under standard atmospheric conditions is roughly 1.2 kg/m 3 . At this pressure and density, breathing 21% oxygen provides the average healthy human body with enough oxygen molecules to support normal cellular functions. In other words, our bodies function well when we are breathing in 400–600 mL of 21% oxygen at a pressure of 14.5 psi and a density of 1.2 kg/m 3 .

Under a variety of medical situations, supplemental oxygen is used as an adjunct to general atmospheric oxygen. This can occur in both acute and chronic situations where the body is unable to maintain normal cellular function by breathing air alone. Whether in an emergency room, on an operating table, or even at home, people use supplemental oxygen therapy in a variety of situations to assist the distressed human body. However, this is all done at a standard atmospheric pressure and density. What happens when that supplemental oxygen is delivered at a higher pressure? What effects would this have on the body? This is precisely what scientists have been exploring for many years with hyperbaric oxygen therapy, or HBOT. Hyperbaric oxygen tanks are enclosed capsules in which patients lie flat and receive 100% oxygen at anywhere between 1 and 3 ata, or one to three times normal atmospheric pressure. The purpose of this tank is to provide the body with an ultrahigh concentration of supersaturating oxygen that would be unavailable using standard supplemental oxygen equipment. HBOT is currently used for a variety of ailments including decompression sickness, cyanide poisoning, and necrotizing infections ( ). Only within the past decade has HBOT gained a reputation as being a possible treatment for trauma to the brain. This chapter will explore the use of HBOT for traumatic brain injury (TBI), as a review of what is already known and what additional information we must gather in recommending its standard use of therapy.

A Brief History of HBOT

At 100 ft beneath the surface, the pressure surrounding a scuba diver is about 43 pounds per square inch. With a standard sea level pressure of 14.7 psi, the pressure at that depth is equal to roughly 3 atm of pressure. While being submerged at 100 ft may not pose any inherent danger to the human body, a rapid fall in pressure could be potentially life-threatening. Inert gases, most notably nitrogen, exist in physical solution in the body at high pressure. A sudden decrease in pressure causes the gas molecules to come out of solution and form gas bubbles in the blood stream and other parts of the body. This is exactly what happens when divers surface too quickly and do not allow their bodies to adjust for these dramatic changes in pressure. Professionally called nitrogen sickness, or decompression sickness, popular culture refers to it as “the bends.” The bends can be a potentially fatal condition depending on where the gas bubbles form in the body and must be treated immediately. The signs of decompression sickness include a wide array of neurological, cutaneous, musculoskeletal, audiovestibular, and pulmonic symptoms such as fatigue, loss of balance, seizures, confusion, itching, and joint pain. HBOT is the most effective means of dealing with the bends and requires placing the body in an environment that recreates the condition in which inert gases exist in solution. The pressure is then slowly lowered in a way to simulate a slow return to surface that prevents the gas bubbles from forming.

The hyperbaric tank has existed for close to 350 years. Though attempts to conjure its design were previously attempted with no success, a British physician named Nathaniel Henshaw achieved the first documented closed “hyperbaric” environment in the 17th century. Stemming from his work in 1662, Dr. Henshaw reportedly filled a small capsule called a domicilium with highly compressed air to create a hyperbaric environment. Henshaw based his work off the principles of the Irish physicist and chemist Robert Boyle, who famously identified the inverse relationship between pressure and volume of air in a closed space. Several 100 years of medical experimentation and development passed before the technology was adopted into mainstream medicine. By the 1870s, hyperbaric tank air therapy was commonly used to treat a variety of ailments with various successes. Due to concerns of oxygen toxicity and limited knowledge of treating such ailments, the original hyperbaric tanks used compressed air instead of oxygen. It was not until 1917 that two German brothers Bernhard and Heinrich Dräger began applying pure oxygen to the tanks, resulting in the first successful treatment for decompression sickness caused by diving accidents ( ).

Hyperbaric therapy did not make its way to the United States until 1861, when neurologist James Leonard Corning saw its potential as a unique therapeutic option. Corning was interested in the technique after witnessing severe decompression sickness among site workers in building the Hudson tunnel. He employed the method to treat their collection of symptoms, which was essentially decompression sickness. In 1921, Kansas City-based physician Orval Cunningham built the first hyperbaric tank in the United States with pure oxygen, in treating patients with the flu. Cunningham thought that because there appeared to be a greater incidence of the flu in states with higher altitudes, he could potentially treat the illness with increased pressure. Stunned by his success, Cunningham went on to build the largest known hyperbaric tank in Cleveland, Ohio. The chamber, referred to as the Cunningham Sanitarium, was five stories tall, and contained twelve beds per story. It was considered the “first attempt in history to house people in such a unique structure” ( ). Due to numerous failures in treating infectious diseases, the chamber was dismantled in 1937.

The use of hyperbaric therapy was widely discontinued for nondecompression-related conditions until 1956, when Dutch cardiac surgeon Ite Boerema used the device to aid in cardiopulmonary surgery. In 1961, Boerema’s colleague, Willem Brummelkamp, reported that infections caused by anaerobic bacteria could not survive in a hyperbaric environment, as was postulated by Cunningham and that hyperbaric therapy could provide adequate amounts of oxygen to kill the bacteria. In 1969, the US Navy reported using HBOT to treat patients 3 months following ischemic stroke ( ). When the neurocognitive tests showed significant improvement, the therapy gained interest as a possible option for treatment of acute stroke. Since its renewal into modern medicine, hyperbaric therapy has been used to treat a variety of conditions including carbon monoxide poisoning, wound healing, various types of bacterial infections, and trauma. Even today, some physicians use HBOT in treating medical conditions including gas gangrene, acute traumatic peripheral ischemia, necrotizing infections, osteoradionecrosis, acute peripheral artery insufficiency, and gas embolism. HBOT is unique in that it is the only nonhormonal therapy used for tissue repair and regeneration ( ), including such disorders as diabetic wounds, chronic refractory osteomyelitis, and actinomycosis. It is noninvasive which makes it very desirable for patients in their treatment of disease ( ).

What Is Traumatic Brain Injury?

Brief History

Perhaps the most notable and infamous incident in the history of traumatic brain injury, or TBI, is that of Phineas Gage. Born in 1823, Gage was a railroad construction worker who experienced severe trauma to the head while assisting in the construction of the Rutland and Burlington Railroad in Cavendish, Vermont. The accident occurred in 1848, when at the age of 25 an unexpected explosion sent an iron rod through Phineas’ head and cranium. The rod was three and half feet long, weighed 13 and a half pounds, and had a diameter of one and a fourth inches. The rod entered just under the left cheekbone and flew vertically through his left hemisphere out the top of his head. It landed roughly 30 yards behind him. Even with the substantial head injury, Gage most likely never lost consciousness, as he shortly thereafter walked himself to the office of the physician of Cavendish, Dr. John Martyn Harlow. Gage even explained to Harlow in great detail what had occurred ( ).

Dr. Harlow treated Phineas’ wounds and allowed him to return home 10 weeks after the accident. In 1849, Phineas felt strong enough to return to his work on the railroad. However, the contractor would not rehire Phineas, due to substantial changes in his personality and disposition. Before the accident, Phineas had been a balanced, hard-working, honest individual with a strong intellect and grounded personality. After the accident, Phineas Gage exhibited profanity, would break down in fitful rage, and paraded around like a clown. He became impatient, crude, and obstinate, resorting to immaturity and inappropriate childlike behaviors. These characteristics prevented him from holding any type of intellectual or professional job. Though little is known about the rest of his life, most historians believe that Phineas went on to work remedial jobs as a carriage driver and doorman. His behavior continued to exacerbate throughout his life, causing him to go from one job to another. In 1860, Gage began experiencing epileptic fits, ultimately killing himself that same year ( ).

The importance of Phineas Gage’s story allows us to understand not merely the physical injury that occurred at the time of the accident, but the psychological and personality changes that developed as a result of the trauma. The long-term effects of trauma can be much more hidden and show up slowly over time as a change in behavior and affect. A favorite in the world of neuroscience, Phineas Gage’s story is the seed that grew into modern day TBI and how to treat this complex increasing disorder throughout the world.

Traumatic Brain Injury

TBI is widely considered to be one of the most damaging and misunderstood conditions to the human body. In fact, many believe it to be the leading undiagnosed brain disorder in the United States ( ). Every year, roughly 2 million people suffer from a traumatic brain experience in the United States. More than 500,000 are hospitalized and 50,000 die due to the severity of the injury and lack of adequate treatment. The cost of hyperbaric therapy in the United States is ∼56 billion dollars per year ( ). People, who play contact sports such as football, engage in potentially dangerous hobbies like motorcycling, and members of the military are more likely to experience TBI. While 70–90% of TBI incidents are considered mild, roughly 25% of people do not recover and develop chronic symptoms such as postconcussive syndrome ( ).

Shortly after a TBI, victims can experience symptoms such as confusion, loss of memory, slurred speech, and even seizures ( ). Those living with TBI can struggle with its devastating effects for days, months, years, or potentially the rest of their lives ( ). The actual trauma occurs due to a sudden physical assault on the head that causes damage to the brain. The damage can be focal, confined to one area, or diffuse, involving multiple areas of the brain. The injury itself can be closed-head or penetrating. A closed-head injury occurs when the head suddenly and violently hits an object, but the object does not penetrate through tissue or the skull. A penetrating head injury occurs when an object pierces the skull and enters the brain, destroying tissue and brain matter ( ). While ischemia can also cause significant damage to the brain, it is not usually caused by blunt external force, and thus will not be examined in this chapter.

The Centers for Disease Control and Prevention estimates ( ) that there were 2.5 million cases of TBI in 2010; that same year, TBIs contributed to the deaths of more than 50,000 people; TBI-related emergency department visits increased by 70% from 2001 to 2010; and 249,000 children were treated for TBI that resulted from recreational or sporting activities in 2009. It is important to identify TBI as quickly as possible in part due to the “second-impact syndrome.” When a patient sustains a second head injury before fully recovering from the first, “It leads to an exaggerated response and carries a 50% mortality rate” ( ). While some drugs have shown neuroprotection in animals after a TBI, none have proven very useful in humans. In fact, the standard of care for TBI today consists of allowing the brain to rest and providing symptom relief, primarily for pain ( ). Improved treatment will come through understanding the physical changes in the brain that occur at the microscopic and molecular levels when the brain is subject to trauma. That understanding is only beginning to emerge ( ).

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