HBOT Therapy in Global Cerebral Ischemia Anoxia and Coma
Paul G. Harch and Richard A. Neubauer
An entry from K.K. Jain’s Textbook Of Hyperbaric Medicine
Hyperbaric oxygen therapy has been used in a number of conditions characterized by global ischemia (as opposed to focal ischemia of stroke), and anoxia, and leading to impairment of consciousness. Conditions such as coma due to brain injury and anoxia associated with drowning and hanging are discussed under the following headings:
Rational Basis of HBOT Therapy
Review of Animal Experimental Studies
Review of Human Clinical Studies
For a discussion of the effectiveness of hyperbaric oxygen (HBOT) therapy in global cerebral ischemia/anoxia and coma, we define HBOT as a medical treatment that uses high pressure oxygen as a drug by fully enclosing a person or animal in a pressure vessel and then adjusting the dose of the drug to treat pathophysiologic processes of the diseases. Like all drugs, the dose of HBOT is crucial and should be customized to each patient’s response. It is dictated by the pathological target and is determined by the pressure of oxygen, duration of exposure, frequency, total number of treatments, and timing of the dose in the course of the disease. As diseases and their pathologies evolve, different doses of HBOT are required at different times. In addition, patients have individual susceptibility to drugs, manifest side effects and toxicity. Unfortunately, the ideal dose of HBOT in acute or chronic global ischemia/anoxia and coma is unknown. The studies reviewed below suggest higher pressures (2 ATA or higher) and lesser numbers of treatments very early in the disease process whereas lower pressures (2 ATA or lower) and a greater number of treatments have been used as the brain injury matures. While this general trend seems justified, the absolute or effective pressures delivered to the patients in these reports may be slightly less than what is stated since many studies do not specify the HBOT delivery system that was employed. For example, an oxygen pressurized chamber has an effective HBOT pressure equal to the plateau pressure administered during the treatment, whereas an air pressurized chamber in which oxygen is administered by aviators mask can achieve a far lower effective HBOT pressure, depending on the fit of the mask and the amount of its air/oxygen leak. In the later cases, the dose of oxygen is less. This concept is particularly important when analyzing the studies in this chapter performed prior to the late 1980s when the aviator mask dominated delivery systems in multiplace chambers.
In reviewing the data in this chapter, it is surprising that HBOT has not enjoyed widespread use for neurological diseases in the United States. This has been partly due to institutional reservations and overt therapeutic nihilism for neurological injuries, both of which are presently waning. To assume that HBOT could have efficacy and benefit when liberally applied to various “accepted” indications, yet have none in the great majority of neurological conditions is perplexing. After all, the brain is enclosed within the same body in the same pressure vessel and is exposed to the same elevated oxygen pressure. To justify this distinction, one would have to postulate that an entire set of pathophysiological processes of brain that are insensitive to HBOT and distinct from those in the rest of the body’s organ systems which are sensitive to HBOT and to which we routinely apply HBOT. This is illogical and unlikely. Such reasoning is indefensible when one considers the “accepted” neurological indications include carbon monoxide poisoning, brain decompression sickness, cerebral air embolism, brain abscess, and cyanide poisoning. We conclude that HBOT should benefit other hypoxic/ischemic conditions of the brain, provided the dose is correct, i.e., target specific.
Other reasons for non-recognition of HBOT in neurological conditions concern methodologies. The standard for proof in scientific medicine has been the randomized prospective controlled double-blinded clinical trial. While some of the studies in this chapter meet this rigor (except for double-blinding), many do not. Some are randomized, prospective, and controlled and thus exceed the quality of studies used to sanction reimbursement for some HBOT indications. Other studies are uncontrolled series, case-controlled, or individual cases. All of this clinical data, in conjunction with the animal data, makes a strong case for at least attempting HBOT in what are otherwise untreatable conditions with debilitating, tragic, and expensive outcomes, especially when the visual medium is used to prove single-case causality (Kiene & von Schon-Angerer 1998; Harch 1996). In addition, case-controlled series with chronic neurological maladies make powerful statements of efficacy from the statistical (Glantz 1992) and logical perspectives where the counterargument of placebo effect is minimized (Kienle & Kiene 1996). If these considerations are kept in mind when analyzing this chapter, it appears that the bulk of data is solidly in favor of a beneficial effect of HBOT in global ischemia/anoxia and coma.
HBOT and the effects on Coma Patients:
Hyperbaric Oxygenation of Anoxic Encephalopathy and Coma
Brief Summaries of References
Presented at XII International Congress on Hyperbaric and Underwater Medicine, Milan, September 1996. 1.* Neubauer RA. The effect of hyperbaric oxygen in prolonged coma. Possible identification of marginally functioning brain zones.
Medicina Subacquea ed Iperbarica. 1985: (3) 75-79. 17 cases of vegetative coma for 1 – 22 months. 40 – 120 exposures over 20 – 90 days. Glasgow Coma Scale improved in all. Complete recovery of 5. 2. * Eltorai I, Montroy,R. Hyperbaraic Oxygen Therapy leading to recovery of a 6-week comatose patient afflicted by anoxic encephalopathy and post-traumatic edema. J.
Hyperbaric Medicine 1991: (3) 189-198. 90 mins HBO od. After 24 sessions, started talking and ate meals. Gradually mobilised to a wheelchair.
3. * Harch PG, et al. SPECT brain imaging and low pressure HBO in the diagnosis and treatment of chronic traumatic, ischaemic, hypoxic and anoxic encephalopathies. Undersea and Hyperbaric Med. 1994 (Supp) 4/5 showed improvement in focal cortical & deep grey matter deficits.
4.* Shn-rong Z. Hyperbaric Oxygen Therapy for Coma – report of 336 Cases.In Proc XI Intnl Cong Hyperbaric Med. Best, Flagstaff. 1995; 279-285 HBO is effective in acute brain hypoxia and oedema and can hasten recovery of consciousness, including prolonged coma.
5. * Neubauer RA. Gottlieb SF, Pevsner NH. Long-anoxic ischaemic encephalopathy: predictability of recovery. In Proc XII Intnl Cong Hyperbaric Med. Best, Flagstaff. 1996. (In press). 8 long-term patients with severe anoxic ischaemic encephalopathy between 3 months and 12 years. Improvement in all cases, both clinically and on SPECT scans. Until the introduction of SPECT scanning there has been no diagnostic technique providing evidence that any treatment would be effective.
6. * Quinly C, Shaoji Y. Nursing of Brain-Stem injury with HBO. Ibid. 39 patients treated with HBO. Decreased mortality and increased awake rate
7. # Zhi Y, et al. Assessment of the efficacy of HBO in patients with a persistent vegetative state. Ibid. 8 patients in coma, longest 281 days prior to HBO. 20 – 86 daily sessions. All resumed consciousness. ———– 414 cases reported, worldwide, in the since 1987.