**2. Background**

On August 30, 2002, Medicare announced its intention to issue a national coverage determination (NCD) for Hyperbaric Oxygen Therapy (HBOT) in the treatment of diabetic wounds of the lower extremities. The arguments that led to that determination [3] established that oxygen under pressure was safe and effective for this fourteenth indication, or disease state.

The evolution in thinking and the subsequent research was enabled by the 1999 refinement and restatement of the drug definition of HBOT as the use of greater than atmospheric pressure oxygen as a drug to treat basic pathophysiologic processes and their diseases [4]. The UHMS defines hyperbaric oxygen (HBO2) as an intervention in which an individual breathes near 100% oxygen intermittently while inside a hyperbaric chamber that is pressurized to greater than sea level pressure (1 atmosphere absolute, or ATA) [5]. With that definition the totality of on-label indications could be understood as cohesive sets of diagnoses connected by HBOT effects on the acute and/or chronic underlying pathophysiology common to the diseases.

Doctors noticed that the definition necessarily could be applied to the use of HBOT for additional diseases that shared this pathology. Of the 14/15 indications accepted by the FDA/CMS, at least five are non-healing wounds and therefore closely related to brain wounding from blast, falls, impact, stroke, Improvised explosive devices, and concussion. Those indications are: Crush injury, compartment syndrome, and other acute traumatic ischemias; Arterial Insufficiency, entailing enhancement of healing in selected problem wounds (includes uses like Diabetic Foot Wounds, Hypoxic Wounds); Radiation tissue damage (soft tissue and bony necrosis); Skin grafts and flaps (compromised); and Air or gas embolism (resulting from rapid decompression and blast injury [6].)

The accurate drug definition of HBOT, and its implications for the findings and data in research into traumatic brain injury, is used in this paper to argue for HBOT safety and effectiveness in the treatment of Traumatic Brain Injury. The argument is constructed by identifying the underlying pathophysiology in traumatic brain injury. Evidence for the beneficial effects of HBOT on TBI is presented. Benefits to patients with TBI is discussed. Evidence for HBOT for TBI risk/benefit and cost/are discussed. The conclusion is simple: coverage of HBOT for TBI.

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*Hyperbaric Oxygenation in the Treatment of Traumatic Brain Injury*

Research over the last two decades has revealed the complex microcosms of multiple pathophysiological processes resulting from insults to the brain, including traumatic brain injury [7]. The three essential components determining the outcome of head injuries are brain blood flow; the pressure in the skull leading to

According to the Centers for Disease Control and Prevention (CDC), "traumatic brain injury (TBI) is caused by a bump, blow or jolt to the head or a penetrating head injury that disrupts the normal function of the brain." TBI severity ranges 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 [9]. The CDC keeps

Traumatic brain injury (TBI) is a major cause of death and disability in the United States. Those who survive a TBI can face effects that last a few days, or the rest of their lives. Among TBI-related ED visits and hospitalizations in 2014,

• Hospitalization rates were highest among persons 75 years of age and older

• For adults 55 years of age and older, falls were the leading cause of hospitaliza-

• Among TBI-related deaths in 2014, rates were highest for persons 75 years of

• Between 2001 and 2010, the estimated average annual numbers of TBI in the US equaled: TBI contributed to the deaths of 56,800 people; 282,000 hospital-

• Accidental traumatic brain injuries contributed to more deaths than suicides

• The lifetime economic cost of TBI, including direct and indirect medical costs, was estimated to be approximately \$76.5 billion (in 2010 dollars) [12].

• Current estimates put the yearly costs of TBI among veterans at \$48 billion [13].

UCLA researchers, citing animal and human studies, speak of "a neurometabolic

cascade of events that involves bioenergetic challenges, cytoskeletal and axonal alterations, impairments in neurotransmission and vulnerability to delayed cell death and chronic dysfunction.. .. linking the neurometabolic cascade to clinical characteristics as well as on new connections being made between acute postconcussion pathophysiology, long-term biological changes and chronic sequelae." [14] Further: "The etiology of postconcussive syndrome is debated, but may be caused by diffuse axonal injury or persistent metabolic alterations resulting in neuronal dysfunction and develops in 38–80% of patients with TBI…." [15].

• Approximately 5.3 M people in the US live with a permanent TBI [11]

• In 2014, an average of 155 people in the United States died each day from

• The highest rates of ED visits included persons 75 years of age and older

*DOI: http://dx.doi.org/10.5772/intechopen.94401*

swelling; and hypoxia, the lack of oxygen [8].

current statistics on TBI death and disability.

statistics notable for the CDC include:

tions and ED visits

injuries that include a TBI

izations; and 2.5 M ER visits.

and homicides together [10].

age and older

**3. Traumatic brain injury basics**
