Neil B.Hampson, Emeritus Physician, Virginia Mason Medical Centerneil.hampson@gmail.com
James Holm, Medical Director
Submitted October 26, 2016
In their article, Drs. Figueroa and Wright reported a reanalysis of hyperbaric oxygen's effect on mild traumatic brain injury and claimed that oxygen content of arterial blood plasma (oxygen dissolved in plasma) during hyperbaric exposure correlates with treatment response. [1]
Arterial blood plasma oxygen content was not measured in any of the studies reviewed. The authors provided no details in the methods, but undoubtedly estimated it from arterial blood partial pressure of oxygen (PaO2, in mmHg oxygen) by multiplying PaO2 by the coefficient 0.0031 mL/mmHg oxygen/dL. However, PaO2 during hyperbaric exposure was not measured in the studies. It was presumably estimated from the calculated alveolar PO2 using the alveolar gas equation and making the assumptions that these subjects had normal metabolism (respiratory quotient) and pulmonary function (alveolar to arterial oxygen difference).
Not only were the authors attempting to correlate the response to a value several estimates or assumptions beyond anything actually measured, they ignored the fact that the studies used different treatment times and numbers. If total oxygen dose administered was calculated (partial pressure of oxygen breathed x minutes of hyperbaric exposure x treatment number), it would not correlate in any meaningful way with clinical response in the reported studies.
1. Figueroa XA, Wright JK. Hyperbaric oxygen: B-level evidence in hyperbaric oxygen therapy trials. Neurology Epub 2016 Aug 31.
For disclosures, please contact the editorial office at journal@neurology.org.
In their article, Drs. Figueroa and Wright reported a reanalysis of hyperbaric oxygen's effect on mild traumatic brain injury and claimed that oxygen content of arterial blood plasma (oxygen dissolved in plasma) during hyperbaric exposure correlates with treatment response. [1]
Arterial blood plasma oxygen content was not measured in any of the studies reviewed. The authors provided no details in the methods, but undoubtedly estimated it from arterial blood partial pressure of oxygen (PaO2, in mmHg oxygen) by multiplying PaO2 by the coefficient 0.0031 mL/mmHg oxygen/dL. However, PaO2 during hyperbaric exposure was not measured in the studies. It was presumably estimated from the calculated alveolar PO2 using the alveolar gas equation and making the assumptions that these subjects had normal metabolism (respiratory quotient) and pulmonary function (alveolar to arterial oxygen difference).
Not only were the authors attempting to correlate the response to a value several estimates or assumptions beyond anything actually measured, they ignored the fact that the studies used different treatment times and numbers. If total oxygen dose administered was calculated (partial pressure of oxygen breathed x minutes of hyperbaric exposure x treatment number), it would not correlate in any meaningful way with clinical response in the reported studies.
1. Figueroa XA, Wright JK. Hyperbaric oxygen: B-level evidence in hyperbaric oxygen therapy trials. Neurology Epub 2016 Aug 31.
For disclosures, please contact the editorial office at journal@neurology.org.