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Hyperbaric Oxygen Therapy (HBOT)

HBOT Scientific Overview
Rescue for Blunt Trauma, Crush & Acute Traumatic Brain Injury
The Use of Hyperbaric Medicine in Acute Trauma
Evidence For Use Of Hyperbaric Oxygen Therapy For Acute Traumatic Brain Injury

Evidence For Use Of Hyperbaric Oxygen Therapy For Acute Traumatic Brain Injury
Download Document: Evidence For Use Of Hyperbaric Oxygen Therapy For Acute Traumatic Brain Injury
Traumatic brain injury (TBI) affects over 1.6 million United States residents annually and a far greater number internationally (Ghajar). Over 50,000 of these individuals will die from their brain injury and greater than 80,000 will have permanent severe neurological disability (Ghajar). Since the development of modern emergency medical system (EMS) management of acute trauma no therapeutic modality has further reduced the mortality of traumatic brain injury. The data below will show that the only modality in the history of science and medicine with a scientifically proven reduction in mortality in acute severe traumatic brain injury is timely low-pressure hyperbaric oxygen therapy (HBOT). Some of this data also suggests a benefit for functional improvement.
Any discussion of the effect of HBOT on a medical condition should be based on the concept of drug dosage. A comprehensive definition of HBOT as a drug is necessary: HBOT is the use of greater than ambient atmospheric pressure oxygen as a drug to treat basic pathophysiologic processes/states and their diseases (Harch, Jain). The dose of HBOT is a function of the fractional percentage of oxygen, rapidity of pressurization and depressurization, depth of pressurization, length of time at depth, frequency of treatments, presence or absence and duration of air breaks and surface intervals, number of treatments, and time of intervention in the natural history of the disease, which identifies the pathological targets. The data in this paper will be discussed and evaluated in terms of dosing and will emphasize the absolute pressure, time at depth, frequency and number of treatments, and time of intervention. The medical literature will be reviewed to first answer the question of efficacy of HBOT on the underlying pathology, pathophysiology, and outcomes of acute TBI in animals and second to see if this efficacy is duplicated and reinforced by the human clinical literature.
TBI is a diffuse cerebral insult characterized by primary mechanical disruption of tissue (Peerless), (Strich), (Adams) and secondary injury from ischemia (Bouma), hypoxia(Adams), (van den Brink), (Zhi), edema (Adams), (Schoettle), (Bullock), vasospasm (Martin), (Zurynski), neurochemicals (McIntosh), (Hovda),and reperfusion injury (Zhuang), (Schoettle). A review of the medical literature shows that there is substantial data proving a beneficial effect of HBOT on the secondary injury processes of acute TBI. HBOT has been shown indirectly to improve ischemia and hypoxia in acute TBI by its effect on aerobic metabolism and EEG. Contreras (ref) recorded a persistent increased cerebral glucose utilization in 5 of 21 areas of brain remote from a cryogenic injury 24 hours after the fourth HBOT. Treatments began 30 minutes after the injury and continued daily at 2 ATA/90 minutes. Holbach (J. Neurol) obtained a similar result in humans with acute severe TBI (23 patients), and stroke (7 patients) a few days post injury/ictus. Measuring the glucose oxidation quotient, he found aerobic metabolism to be maximal in injured brain at 1.5 ATA. A single 10-15 minute excursion to 2.0 ATA had a toxic effect on glucose uptake and metabolism that persisted after return to room air. Holbach (6th Int. Congress) reinforced this finding by demonstrating simultaneously improved EEG and decreased regional cortical blood flow (rCBF) in a similar or the same group of acute severe TBI patients at 1.5 ATA. Upon presure increase to 2.0 or 2.5 ATA for 30 minutes EEG markedly deteriorated and rCBF increased significantly. Some patients experienced persistence of these toxic effects upon return to room air.
HBOT also has beneficial effects on vasospasm. Yufu showed that 30 minutes after sub-arachnoid hemorrhage a single HBOT at 2.0 ATA/60 minutes reversed reductions in Na+, K+-ATPase activity and cell membrane alterations. Similarly, Kohshi documented a clinical benefit of
HBOT on vasospasm in a controlled human study. He found that HBOT at 2.5 ATA/60 once or twice/day (average 10 treatments) soon after symptomatic vasospasm in post-op SAH/aneurysm patients decreased strokes and improved neurological outcome and EEG over controls.
Multiple studies have shown that HBOT reduces cerebral edema and decreases ICP. Coe used a single 3.0 ATA/120 HBOT immediately after cryogenic brain injury in rats to improve neuronal destruction, cerebral edema, and length of survival from 2 hours to 12.5 hours. Coe reinforced these results with a follow-up percussion brain injury experiment. He showed that a single 3.0 ATA/60 HBOT with 2% carbogen immediately after injury resulted in a significant improvement in maze running ability over controls at seven days that was nearly equal to non-injured animals. Sukoff (1968), using cerebral implantation of psyllium seeds in dogs, delivered HBOT beginning 24 hours after surgery at 3.0 ATA/ 45 (total dive time?) three times/day tapering to once or twice/day, and found a reduction in cerebral edema and cisternal fluid pressures and an increase in survival. In another model of cryogenic injury Miller, Ledingham, and Jennett showed that a single HBOT at 2.0 ATA/15-30, beginning minutes after injury, reduced ICP, but at 40-60 minutes the reduction in ICP began to reverse and rebounded (in some dogs) above baseline on return to air breathing. With the same model Miller and Ledingham later showed that HBOT at 2.0 ATA/4 hours, beginning one hour after injury, caused an initial reduction in ICP that progressively reversed and then significantly rebounded post HBOT. Simultaneously, CSF lactate increased to the levels of controls, contrary to Holbach’s experiment above. A third experiment by this group in the same model confirmed the benefit of short exposures of HBOT at 2.0 ATA. Dogs subjected to 2.0 ATA/15 had a 33% reduction in ICP and an improvement in perfusion pressure while dogs at 3.0 ATA/15 had a reversal of ICP reduction and rebound after return to surface, indicating a toxic effect of this pressure. Kanshepolsky subjected cats to cryogenic brain injury and treated with HBOT at 2.5 ATA/90 three times/day for upto three days, beginning either two or 6 hours after injury. HBOT increased survival and decreased brain edema if begun two hours after injury, but had no significant effect if treatment was delayed to six hours. A summary of the HBOT/cerebral edema studies in animals is that HBOT has two different effects (Hayakawa): 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 (Holbach). If not reversed seizures follow (Bean), (Chavko). It appears that high pressures (greater than or equal to 2.0 ATA) maybe beneficial for very short periods of time (15-30 minutes) if delivered within a few hours after acute brain trauma. A similar conclusion has been reached in global ischemia/anoxia/coma (Harch, Jain). These pressures, however, have a toxic effect if used for greater duration and beyond the 2-3 hour post injury period. During this later period 1.5 ATA/30 minutes appears to be the optimal pressure/duration (human data).

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