Problem wounds represent the most common use hyperbaric oxygen (HBO) therapy, by some estimates constituting greater than 80% of all rendered treatments. Despite this long-established indication, however, no standardized treatment pressure exists. Authoritative guidelines recommend 2.0-2.5 ATA, with clinical practice commonly employing 2.0, 2.36, 2.4 or 2.5 ATA. While none of these pressures has been proven therapeutically superior, important patient and health care worker safety concerns associated with increasing pressures argue for employment of the lowest clinically effective pressure.
The genesis for this pressure range appears to have been the development of a clinical hyperbaric medicine program using the multiplace chamber at the U.S. Air Force School of Aerospace Medicine, San Antonio, Texas, in the early 1970’s. Existing literature was searched for a suitable wound enhancement protocol. Practitioners in Europe and elsewhere in the U.S. were noted to be successfully employing a hyperbaric oxygen pressure of 2.0 ATA to treat post-radiation soft tissue wounds, radiation damaged facial bones, refractory osteomyelitis, compromised skin flaps and ischemic ulcers. I purposely emphasized the word oxygen, and the reason will become soon apparent. Almost exclusively, these reports were associated with oxygen filled monoplace chambers.
Air compressed multiplace chambers require an individualized oxygen delivery device, traditionally an aviator type oral nasal mask. The USAF team recognized that a multiplace chamber pressure of 2.0 ATA would fail to produce an oxygen pressure of 2.0 ATA, given mask delivery system shortcomings (Sheffield PJ, at al. 1977; later corroborated by Stephenson RN, et al. 1996).
Development of the multiplace chamber treatment pressure
In order to ensure that a prescribed oxygen dose of 2.0 ATA could be achieved during multiplace operations the USAF team empirically proposed that the chamber be compressed to 2.5 ATA. This was quickly rejected, however, as it represented 49.5 fsw on the chamber pressure gauge. The problem this represented was that any minor overshoot (secondary to operator error and/or effect of chamber warming) would place the inside attendant (IA) on the 60 fsw air decompression table. Their resulting available ‘bottom time’ would become significantly less that the planned patient treatment time. A compromise was reached by electing to compress to 45 fsw ‘as it was an easy mark on the gage (sic) for the technician to maintain’. (Sheffield PJ, 2004). This represented an air chamber pressure of 2.36 ATA so at least 2.0 ATA oxygen was assured, based upon the above cited mask analysis data. Subsequent clinical reports from this facility invariably rounded up 2.36 to 2.4 ATA for simplification purposes. The influence of the USAF program was such that this multiplace chamber pressure became commonplace, and on an international scale. Elsewhere, others had elected to employ 2.5 ATA, in part because this pressure was already being used to treat acute conditions at their respective facilities.
The basis for this now widely adopted multiplace chamber pressure was, therefore, a somewhat arbitrary method to ensure provision of at least 2.0 ATA oxygen. (Sheffield PJ, 2004)
Multiplace chamber inside attendant decompression sickness
It has long been appreciated that health care workers who accompany patients during multiplace chamber treatments are at risk for iatrogenic decompression sickness (DCS). Admittedly, overall incidence is low, when calculated as number of cases over number of exposures, or the potential for a case to occur during any given exposure. Employee cumulative risk, however, defined as number of cases over number of available IAs, or the potential for a given inside attendant to suffer DCS, is high, exceeding 80% in one report. (Dunford RG & Hampton NB, 1992) The issue of IA decompression sickness has recently been comprehensively reviewed (Clarke R, 2017). Such decompression accidents have resulted in at least two nurse deaths, a considerable number of spinal cord injuries, some permanent and career-ending, and many less severe and fully recoverable manifestations.
Importantly, a linear correlation exists between increasing chamber pressure and increasingly DCS incidence. (Dunford RG & Hampton NB, 1992; Dietz SK, et al. 1995; ECHM Consensus Conference 2003).
A disturbing number of IA DCS cases secondary to 2.4 ATA exposure had occurred at Memorial Hermann Hospital, Houston, Texas. This led to a switch from the traditional oral nasal mask to a hood delivery system, thereby assuring 100% oxygen delivery, with all subsequent treatments being rendered 2.0 ATA. (Fife, CE. Unpublished document/personal communication 2017) There have been no reported IA DCS cases since. This same oxygen delivery system switch/pressure reduction has been implemented at multiplace facilities elsewhere, again with no subsequent reported cases of IA DCS and no apparent degradation in clinical outcomes.
Patient central nervous system oxygen toxicity
A second issue is that of oxygen toxicity, where again a linear correlation exits between increasing chamber pressure and increasing rates of toxicity. In one report that uniquely included a 2.0 ATA treatment protocol assessment, a pressure of 2.0 ATA resulted in no seizures per 10,000 exposures, while15 seizures were recorded per 10,000 exposures involving 2.4/2.5 ATA. (Heyboer M, et al. 2014) This blog’s writer did witness one seizure at 2.0 ATA, although it is an exceedingly rare event based upon published literature.
Clinical efficacy of 2.0 ATA
The final and perhaps most crucial issue in all of this is clinical efficacy. Namely, is treatment at 2.0 ATA oxygen suitably therapeutic for the problem wound patient? The short answer is that indeed it is. The first highest quality evidence-based study conducted to assess the effect of HBO therapy in deficient wound repair, in this case pelvic soft tissue radio-necrosis, demonstrated a statistically significant healing effect using 2.0 ATA oxygen. (Clarke R, et al. 2008) Further, in the U.S., monoplace chambers dominate delivery of HBO therapy and their common treatment pressure is 2.0 ATA, with nothing to suggest that this oxygen pressure is not having the desired effect, on the contrary.
An animal model did demonstrate an almost linear angiogenic dose response curve as chamber pressure was increased, up to 3.0 ATA, where the experiment was halted. (Ehler WJ, et al. 1993) These authors made no attempt to consider the optimal balance between therapeutic benefit and associated risks. One of this paper’s authors did, however, suggest elsewhere that 2.0 ATA was a ‘clinically acceptable’ dose. (Marx RE, 1990).
The era of the 1960s - 1970s saw the introduction of HBO therapy as successful treatment for a number of chronic healing deficient states. The oxygen-filled monoplace chamber commonly served in this capacity, utilizing an almost uniform 2.0 ATA chamber pressure (thereby affecting a 2.0 ATA oxygen dose). With the introduction of the USAF multiplace chamber for wound healing enhancement, a slightly higher chamber pressure was employed to accommodate for the observed chamber pressure - oxygen pressure mismatch, secondary to mask oxygen delivery shortcomings. It was never this group’s intent to deliver a 2.36 ATA oxygen dose.
With the advent of the more effective patient hood for multiplace patient oxygen delivery, there is no longer a requirement to compress beyond 2.0 ATA as the referenced mismatch is eliminated. Several multiplace programs have readily grasped this concept. They now treat at 2.0 ATA chamber pressure using hoods, some having been further prompted by IA decompression incidence/risk and patient toxicity. In doing so, they have largely eliminated both safety concerns. Those programs continuing to use the higher pressure with hood oxygen delivery would be well served to reconsider their protocol in light of this narrative. Others who continue to use masks would be equally well served to switch to hoods and the lower chamber pressure, not least to enhance patient and IA safety.