There were errors in the article by Rose and colleagues (1), which appeared in the March 1, 2017 issue of the Journal. In Table 1, “Intervention” column, the second entry for Reference 83 should read “LOC: 2× HBO2 (2.0 ATA) × 60 min” instead of “90 min.” In addition, for the row corresponding to Reference 87, the numbers in the “Events Treated” and “Events Control” columns should be reversed: “33/79” should appear under “Treated,” and “29/74” should appear under “Control.” For the convenience of our readers, we reprint the corrected table below (Table 1) (the corrected figures appear in boldface).
Table 1.
Hyperbaric Oxygen Trials versus Control Shows Mixed Evidence of Benefit
| Reference No. | Intervention | Reference | Evaluation | Events |
Benefit | |
|---|---|---|---|---|---|---|
| Treated | Control | |||||
| 83 | No LOC: HBO2 (2.0 ATA) × 60 min | NBO2 6 h | Neurologic symptoms at 1 mo | 51/159 | 50/158 | N |
| LOC: 2× HBO2 (2.0 ATA) × 60 min | 1× HBO2 (2.0 ATA) × 90 m | |||||
| 84 | HBO2 (2.8 ATA) × 30 min | NBO2 until asymptomatic | Delayed neurologic sequelae 4 wk follow-up | 0/30 | 7/30 | Y |
| then (2.0 ATA) × 90 min | ||||||
| 85 | HBO2 (2.5 ATA) × 90 min | 12 h NBO2 | 1 mo persistent neurologic symptoms | 69/299 | 73/276 | N |
| 86 | HBO2 (2.8 ATA) × 100 min × 3–6 d | NBO2 × 100 min sham for 3–6 d | Neuropsychologic testing 1 mo | 34/52 | 20/34 | N |
| 82 | HBO2 1× (3 ATA × 1 h; 2 ATA × 1 h) then 2× (2 ATA) × 90 min | NBO2 sham treatment | Cognitive sequelae at 6 wk, 6 mo, and 1 yr | 19/76 | 35/76 | Y |
| 87 | HBO2 (2.0 ATA) × 60 m, NBO2 × 4 h | NBO2 6 h | Neurologic assessment 1 mo | 33/79 | 29/74 | N |
| 88 | LOC: HBO2 (2.0 ATA) × 1 h + 4 h NBO2 | NBO2 6 h | 1 mo questionnaire + physical exam | 33/93 | 29/86 | N |
| Coma: 2× HBO2 (2.0 ATA) 1x h + 4 h NBO2 | 1× HBO2 + 4h NBO2 | 42/105 | 25/101 | N | ||
| 89 | HBO2 (2.5 ATA) x2 h + 10 h NBO2 | NBO2 × 12 h | 3 wk EEG impairments or not | 0/8 | 6/10 | Y |
Definition of abbreviations: ATA = atmospheres; HBO2 = hyperbaric oxygen; LOC = loss of consciousness; N = no; NBO2 = normobaric oxygen; Y = yes.
A metaanalysis (90) concluded that there is no clear benefit to HBO2 in terms of delayed neurologic sequelae; however, with the significant heterogeneity in outcome measures and the treatments themselves, it is difficult to draw conclusions from metaanalyses on HBO2.
At the time of the acceptance of the manuscript (October 14, 2016), some of the authors were co-inventors on pending U.S. patent applications directed to the treatment of carbon monoxide poisoning; however, this information was not included in the ICMJE disclosure forms attached to the online article. At that time, the AJRCCM Instructions for Contributors did not specify that pending patent applications should be listed on the disclosure forms (subsequently, the instructions have been updated to explicitly request the disclosure of all patents held or pending). We include here the patent/conflict positions at the time of the original ahead-of-print publication of the article (October 18, 2016), as supplied by the authors:
Dr. Rose, Dr. Xu, Dr. Tejero, and Dr. Gladwin are co-inventors of pending provisional patent applications and planned patents directed to the use of recombinant neuroglobin and heme-based molecules as antidotes for CO poisoning. Additionally, and unrelated to CO poisoning, Dr. Gladwin is a co-inventor on patents directed to the use of nitrite salts in cardiovascular diseases.
Reference
- 1.Rose JJ, Wang L, Xu Q, McTiernan CF, Shiva S, Tejero J, Gladwin MT. Carbon monoxide poisoning: pathogenesis, management, and future directions of therapy. Am J Respir Crit Care Med. 2017;195:596–606. doi: 10.1164/rccm.201606-1275CI. [DOI] [PMC free article] [PubMed] [Google Scholar]
