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350 years of hyperbaric medicine: historic, physiopathologic
and therapeutic aspects
Oswaldo Huchim1, Fernando Rivas-Sosa2, Normando Rivera-Canul3 and Nina Méndez-Domínguez3
1Unidad Experimental Marista; 2Hospital General O’Horan; 3Universidad Marista de Mérida. Mérida, Yucatán, Mexico
Gac Med Mex. 2017;153:854-860
Contents available at PubMed
www.gacetamedicademexico.com
Abstract
The early use of hyperbaric therapy started with the quest to relieve respiratory problems among inhabitants of large cities
during the industrial revolution, and from this, we have explored the benefits of treatment with hyperbaric oxygen in different
areas of medicine. With the advances of the medical sciences, our knowledge concerning the therapies with hyperbaric oxy-
genation certainly has broadened and hyperbaric medicine still intrigues the contemporary medical researchers that are in seek
of improve the quality of life of their patients.
KEY WORDS: Hyperbaric oxygenation. Decompression sickness. Atmospheric pressure. History of medicine. Therapeutics.
Physiopathology.
Date of reception: 12-12-2016
Date of acceptance: 04-01-2017
DOI://dx.doi.org/10.24875/GMM.M18000102
Gaceta Médica de México HISTORY AND PHILOSOPHY OF MEDICINE
Introduction
Hyperbaric oxygenation provides a therapy mainly
intended for the treatment of decompression sickness,
generated by changes in environmental pressure, as
it occurs in the case of diving and aeronautics. In a
second place, hyperbaric oxygenation is used for
cosmetic purposes, owing to its popularized use to
counteract cell aging. However, hyperbaric medicine
offers much more than this and is, with no doubt, a
useful resource during the comprehensive treatment
of various pathologies that involve ischemic
processes.
Hyperbaric oxygenation can have several applica-
tions both in emergency situations and to potentiate
the effect of comprehensive therapies in chronic pa-
thologies or acute events’ sequels. The purpose of
the present article is to review the history and patho-
physiogenic mechanisms involved in hyperbaric
therapy.
Background
Oxygen, as other gases, reacts with pressurization
and depressurization; when oxygen concentration
increases owing to its solubility under pressure, its
diffusion gradient is increased, which enables deep
penetration into tissues. It is by this principle that the
treatment with hyperbaric oxygenation helps in the
repair of poorly perfused, hypoxic, ischemic, infarcted
or necrotic tissue areas. Better oxygenation enables
the triggering of the tissue recovery process and, in
addition, it facilitates reperfusion and angiogenesis.
Hyperbaric oxygen effect on the treatment of differ-
ent health conditions could be known thanks to
experiments carried out in hyperbaric chambers with
diverse animal models1.
Pathologic conditions involving ischemia improve
with hyperbaric oxygen treatment, since this method
consists in 100% oxygen inhalation inside a hyperbar-
ic chamber under pressure, usually at between 2 and
Correspondence:
Nina Méndez-Domínguez
Periférico Norte Tablaje Catastral 13941 Carretera
Mérida- Progreso
C.P. 97300, Mérida, Yuc., México
E-mail: ninuxka@hotmail.com
No part of this publication may be reproduced or photocopying without the prior written permission of the publisher. © Permanyer 2018
O. Huchim, et al.: History of hyperbaric medicine
855
3 atmospheres. As in any treatment, hyperbaric cham-
ber sessions imply dosing both in terms of pressure
and in the number and duration of sessions. Dosing
should be indicated according to the medical condi-
tion to be treated, its seriousness and time of
evolution2,3.
There are two types of hyperbaric chambers: mono-
place or multiplace. While in the monoplace chambers
pressurization occurs by means of oxygen and pres-
sure increase is systemic, multichamber chambers
are pressurized with air and oxygen is supplied with
a facemask, a helmet or and endotracheal tube, as
appropriate4.
Methodology
A review was conducted from the 18th century on,
where historical texts and manuscripts, digitalized by
university libraries, were analyzed. Documents related
to topics associated with barometric, climatic and
topographic characteristics of health and disease pro-
cesses were included, but also the conceptual bases
for the knowledge of the physiological properties of
gases in the human body. The search for articles
published since the 18th century was performed in
PubMed and included the terms “caisson disease” or
“hyperbaric oxygen therapy”, with 651 registries being
obtained, among which those addressing different dis-
eases or syndromes treated with hyperbaric oxygen
therapy were selected, with those that were more
recent and had the highest level of available evidence
(articles based on expert opinions have the lowest
level of evidence, followed by case reports, original
articles, descriptive reviews, systematic reviews and
meta-analyses) being preferred to be included in the
present review.
Physical and physiological bases of
hyperbaric oxygenation therapy
Hyperbaric oxygen therapy effects are based on
biochemical processes that are triggered by hyperox-
ygenation and by physiological effects that are fa-
vored according with physical laws and with the prop-
erties of gases.
In the human body, oxygen is largely transported by
the blood tissue, bound to hemoglobin. In addition, a
proportion of oxygen is transported as a solution, and
this proportion of oxygen can be increased and im-
prove tissue oxygenation according to the principles
outlined in Henry’s law4,5.
Henry’s law establishes that the amount of gas dis-
solved in a fluid or tissue is proportional to the partial
pressure of said gas in contact with the fluid or tissue.
This is the basis to understand the growing pressures
of oxygen in the tissue when hyperbaric oxygen ther-
apy is received. This law also has implications in the
pathophysiology of decompression sickness, since it
affects inert gases (especially nitrogen) tissue con-
centrations as well, which generates effects on the
concentration of said gas in the presence of baromet-
ric changes, thus eliciting an arterial embolism if
reuptake in solution is not achieved5-7. At room tem-
perature, oxygen is at a concentration of 97%. When
breathing normobaric oxygen, oxygen arterial pres-
sure is 100 mmHg, while its tissue pressure is
55 mmHg, and in each liter of blood, there are approx-
imately 3 mL of oxygen available. When breathing
100%m oxygen at 3 absolute atmospheres, oxygen
arterial and tissue pressures increase to 2000 and
500 mmHg, respectively, thus allowing that for each
liter of blood there are 60 mL of oxygen available. In
response to this high amount of oxygen available,
body tissues could potentially remain oxygenated
even in the absence of hemoglobin-transported oxy-
gen. This way, hyperbaric oxygenation allows for
those zones of damaged tissue to be oxygenated,
even if the passage of blood is obstructed or when
red blood cells are incompetent to transport oxygen
by itself, as in the case of poisoning with carbon mon-
oxide and anemia gravis; in addition, it enables oxy-
genation independently of hemoglobin transport in
cases where there is microvascular damage, as it
occurs in diabetes8 -10.
Oxygen captured by respiration also varies during
hyperbaric chamber treatment since, during the de-
scent to deepness, oxygen intra-alveolar pressure in-
creases; this occurs as a physiological response
Boyle’s law and Dalton’s law. Dalton’s law outlines
that, at constant temperature, the pressure of a gas
is inversely proportional to its volume, whereas Dal-
ton’s law states that, in a mixture of gases, each
element exerts a pressure that id proportional to its
fraction of total volume; these laws explain the effect
of oxygen partial pressure and its intra-alveolar
disposition11-14.
In infections, free-radicals act oxidizing proteins and
membrane lipids, which damages the DNA and bac-
terial metabolic functions. Hyperbaric oxygen therapy
increases free radical concentrations, and this is why
it is particularly effective against anaerobic microor-
ganisms by promoting the oxygen-dependent
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Gaceta Médica de México. 2017;153
856
peroxidase system; this system is used by leukocytes
to attack bacteria. Furthermore, it also improves the
transport of oxygen-dependent antimicrobials, allow-
ing their penetration through the cell walls, thus con-
tributing to and potentiating their efficcay15-18.
In tissue lesions, particularly in compartmental syn-
dromes, compression lesions, flaps and lacerations,
leukocytes tend to direct and adhere to damaged tis-
sues to release free radicals and proteases during
reperfusion but, paradoxically, this process can lead
to pathological vasoconstriction causing tissue de-
struction mediated by hypoxia. Similar process occurs
during the neuronal and cardiac ischemia-reperfusion
process during infarctions. There is evidence that hy-
perbaric oxygen reduces leukocyte adherence and
post-ischemic vasoconstriction, which results in better
perfusion of ischemic areas, while favoring oxygen-
ation even in the absence of good perfusion. Another
mechanism by means of which hyperbaric chamber
treatment favors the healing of ischemia-perfusion le-
sions is by amplifying oxygen gradients in the periph-
ery of ischemic lesions, thereby promoting angiogen-
esis, which requires the formation of collagen matrix,
which in turn is oxygen-dependent. Finally, hyperbaric
oxygen therapy enables blood flow redistribution ow-
ing to gradient differences, which alleviates edema
generated in damaged tissues, thus reducing pain and
improving the function19-23 .
It is mainly because of the physical laws here ex-
posed, and the physiological and pathophysiological
pathways involved, that hyperbaric medicine offers
benefits for health conditions involving said pathways.
History
The birth of hyperbaric medicine goes back, as ev-
ery finding, to observation and analysis, in this case,
of the difference in physiological and health aspects
of human populations living in the different geograph-
ical zones24-26.
Arbuthnot, circa 1655, mentioned the relationship
between humidity and the efficiency of air inspired in
different places of the world. For the decade of 1660,
in England, the Industrial Revolution and the emission
of gases by factories with machines operating with
steam and carbon generated concerns in men of sci-
ence and doctors of those days. It was since that
moment that a growing awareness was born that air
pollution was having effects on human health and
wellbeing. Authors such as Digby, in 1658, indicated
among their therapeutic recommendations moving out
from London to those who had “weak lungs, but high
income”, to avoid carbon-polluted air27,28.
Nathaniel Henshaw, and English doctor and clergy-
man, member of the then nascent Royal Society,
aware of the atomist theory, of meteorology, which
was founding its bases in those days, and integrating
knowledge of atmospheric science with the principles
of Boyle’s law, was able to explain the differences he
had identified in the status of health of people living
outside the cities, and believed he had found a rela-
tionship between the weather and altitude of the place
of residence and human health and disease
profiles13,25.
Henshaw, circa 1662, constructed a domicilium,
which consisted of a chamber with a pressurized bel-
lows with a mechanism of piped with valves that, when
manipulated, allowed or limited the passage of the air
contained in the chamber, by means of which he could
control the chamber inner pressure. In this primitive
hyperbaric chamber, the first treatments based on
hyperbaric air were offered with the purpose to pro-
vide poor air to the patients and treat tissues with
purulent secretions or “miasmas”. Thomas Sprat ad-
dressed Henshaw’s work in his book on the knowl-
edge generated by the Royal Society, in 173424,29,30.
Another study of the epoch with important repercus-
sions in the development of hyperbaric oxygenation
was the one by Joseph Black in 1750, who, in assays
with mice, isolated common air carbon monoxide. By
1772, Rutherford discovered nitrogen, and later, in
1774, Priestly was the first one to find and leave a
written report about his transcendent discovery:
oxygen29,31.
Originally, Priestly was trying to generate “dephlo-
gisticated air”, since in his epoch it was thought that
this way the “flammable” characteristics would be re-
moved from the air. This belief was based on the
“phlogiston theory”, which in turn was based on the
flammable properties of a hypothetical substance that
was thought to be part of common air. Thanks to
Priestly, the existence of phlogiston could be discard-
ed, this way preparing the way for pneumatic chemis-
try. According to his registries, when experimenting
with a murid model, the mouse managed to recover
from an aggression with fire “much better” than if it
would have breathed common air. Subsequently, La-
voisier was the first one to name oxygen and to de-
scribe its role on combustion, which may have dis-
couraged physicians of his time about the use of said
gas, in spite of the beneficial effects described by
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O. Huchim, et al.: History of hyperbaric medicine
857
Priestly. In 1794, the first hyperbaric oxygen therapy
center was reported32,33.
It is probable that the first hermetically sealed was
the idea of Cochrane in 1830, wit it was patented until
1839 by Trigger, who designed it to avoid decompres-
sion sickness in French miners, and hence the cham-
bers were known with their French name caisson. In
1834, Williams defined the “caisson disease”, caused
by barometric changes in high places and deep plac-
es, which generate the formation of bubbles and air
embolism, defining it as divers’ disease in his aero-
therapeutics treaty, which addresses health and atmo-
spheric pressure; planes for the manufacturing of
chambers are therein included. In 1857, Paul Bernard
described oxygen affinity for hemoglobin, with the
demand for hyperbaric oxygenation services in Eu-
rope and the USA being triggered on that epoch.
These services were initially provided to heal lesions,
cure infections and improve the respiratory function,
and immediately they became spaces for cosmetic
care, and were even frequented by singers to pre-
serve their tone of voice. In his text, he included the
diagrams and plans of the chambers available on his
epoch, as well as their functioning1,32,34-38.
The first construction of a chamber for laborers
working in the construction of a bridge goes back to
1859 in Rochester, England, by Wright and Hudges.
The track for the subway and the Hudson River Bridge
in the USA started with the construction of the main
tunnel in 1872 by A. Roebling. Both Brooklyn bridge
granite foundations were built by laborers who de-
scended in wooden platforms, submerging to up to 44
feet on the Brooklyn side and 78 feet on the New York
side. Initially, laborers descended without taking pres-
surization into account, but serious consequences
were soon to be observed owing to decompression
sickness. In that moment, little was known about the
risks of working under that conditions, and more than
100 workers suffered decompression sickness. Wash-
ington Roebling himself experienced a gas embolism
that left him partially paralyzed for the rest of his life.
When this problem was identified, boxes started being
used instead of platforms for the descent. The boxes
consisted of chambers or compartments, each one
with different pressure, which enabled the individual
to gradually pass from one to another, maintaining the
doors hermetically closed, and thus avoid abrupt
barometric changes that lead to decompression.
Brooklyn bridge doctor, Adam Smith, picked up the
term caisson disease and defined a preemptive tech-
nique and the decompression cases in 1871 and
1873, describing manifestations such as epigastric
pain and neurological involvement. On May 24, 1883,
Emily Roebling took the first stroll on the finished
bridge with a rooster as a symbol of victory; this
marked the end of the Brooklyn bridge construction
and the beginning of the construction of increasingly
complex hyperbaric chambers3 8- 41.
Between 1904 and 1940, different works related to
decompression sickness were published, with body
fat, and hence obesity, being identified as a risk fac-
tor; in addition, the tissue damage caused by decom-
pression was described according to the type of af-
fected organs, with hyperbaric oxygen therapeutic
effect being emphasized. In 1937, Behnke and Shaw
successfully treated decompression sickness and
subsequently carbon monoxide poisoning; in those
days, the most prominent was the one of Cunning-
ham, in Kansas, registered in 1952. As of 1956, there
was a resurgence of hyperbaric medicine, with tem-
perature control inside hyperbaric chambers, which
enabled oxygenating the patients and keeping them
warm during heart surgeries for acute processes, and
even congenital heart disease repair. Between 1960
and 1977, an estimate of 187 open heart surgeries
were performed, which is so far the only approved
indication for the use of hyperbaric therapy42-47.
Owing to the interest on standardizing and reaching
an agreement on the uses of hyperbaric oxygen, in
the decade of 1970, the Undersea and Hyperbaric
Medical Society (UHMS) was formed, which is the one
that currently issues guidelines with regard to this
therapy4.
By the end of the 20th century, excessive caution
owing to the lack of knowledge about the real mech-
anisms operating in hyperbaric therapy was thought
to be the cause of its underuse in cases where it
certainly might offer benefits to patients, and by 1990,
the body of evidence on its use was rapidly growing,
thus enabling a better understanding of hyperbaric
therapy mechanism of action and potential benefits.
For the first decade of the 21th century, given the con-
cerns of doctors about the use of hyperbaric therapy
due to the controversy that had been generated, the
UHMS issued a list of the 13 approved uses for hy-
perbaric therapy. Even when it is true that there are
pathophysiological processes where hyperbaric oxy-
gen mechanism of action is still poorly known, the
health conditions where hyperbaric oxygen therapy
has been employed in hypobaric medicine modern
epoch will be described next48,49.
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Gaceta Médica de México. 2017;153
858
Background of treatment with hyperbaric
oxygen
The growing population with overweight, obesity,
dyslipidemia and diabetes mellitus often develops se-
quels, and many of them are derived from hypoperfu-
sion and peripheral neuropathy. Owing to the lack of
adequate microcirculation and innervation in the ex-
tremities, diabetes mellitus often generates the forma-
tion of ulcers known as “diabetic necrobiosis”. It is
described in scientific literature that glycemic imbal-
ance-derived ulcers can be alleviated and even healed
with a comprehensive treatment that involves ses-
sions with oxygen in the hyperbaric chamber50-54.
In addition, hyperbaric oxygen often improves reper-
fusion, which favors angiogenesis even in small arter-
ies, such as the retinal artery, the flow of which is
commonly affected by diabetes; therefore, the hyper-
baric chamber can offer benefits to patients with reti-
nopathy of diabetic and non-diabetic etiology, as well
as with retinitis pigmentosa55-57.
Such as hyperbaric oxygen improves oxygenation
and favors circulation in small areas of the body, it has
also been shown to be effective in the ear, helping to
the recovery of two important functions that occur in
the auricular area: hearing and balance. This has been
found both in people with hearing acuity deterioration
and in those who suffer from tinnitus58- 61.
By improving perfusion and favoring some neuro-
sensory aspects, hyperbaric oxygen therapy has been
found to be useful in the recovery of patients who
suffer atherosclerotic strokes, as well as in those who
suffer neonatal hypoxia-related cerebral palsy62- 63. In
certain more complex conditions, as it is the case of
Parkinson disease and carbon monoxide poisoning,
cognitive function has been able to be improved in
subjects who have suffered this type of damage64-66.
In general, it provides benefits to patients who suffer
damage to the nervous system, even in the case of
viral neuropathies, such as those generated by the
herpes zoster virus, or in cases where cerebral dam-
age of the recurrent and chromic type, or caused by
brain tumors. Hyperbaric oxygen therapy has shown
positive effects on the quality of life and function of
pediatric patients with disorders of the autistic
spectrum65-69.
Hyperbaric oxygen benefits have been explored in
the oncological area, with good results being found as
a treatment concomitant with radiotherapy, chemother-
apy or phototherapy, and after tumor-resection thera-
pies, including mastectomy70,71. These hyperbaric
oxygen effects are directly associated with the capac-
ity to regenerate damaged tissues or in healing pro-
cess; it is precisely because of this that it is also useful
in the closure of accident-derived postoperative flaps,
even including scalp closure in at least one individual
who suffered the detachment of this area of tissue72,73.
In addition, an improvement in bladder function has
been found in patients with hemorrhagic cystitis sec-
ondary to radiotherapy treatment74.
Soft tissues damaged by different aggressions can
show an important improvement with the hyperbaric
chamber treatment as well, even if there are data
consistent with infection or gangrene, or if the latter
is of the gas type and generates compartmental
syndrome or fascitis75-77. In cardiac tissue, hyperbaric
oxygen therapy has served to recover ischemic zones
in infarctions, since it favors post-ischemia-reperfu-
sion oxygenation. The same favorable effect of hyper-
baric oxygenation that has been observed in the myo-
cardium has also been seen in pulmonary tissue78,79.
In bone tissue, the effectiveness of hyperbaric oxy-
gen has been previously shown in bone lesions and
as co-adjuvant in cardiothoracic surgery with sternot-
omy, as well as in osteonecrosis secondary to sur-
gery-related trauma or to the consumption of
bisphosphonates68,80.
In some conditions, either acute or chronic, where
toxins that are poisonous to the body need to be
cleared, treatment in the hyperbaric chamber is use-
ful; such is the case of carbon monoxide poisoning,
which may be generated by exposure to emissions of
motor vehicles that use gasoline, just to give an ex-
ample, or by venom inoculated by venomous animals,
such as snakes81,8 2.
Finally, hyperbaric oxygenation beneficial effects
have been reported in hematologic treatments, where
it favors oxygenation and improves blood circulation,
as it occurs in cases of severe anemia and in blood
dyscrasias, such as purpura fulminans83-85.
Its experimental use for the treatment of certain
types of infertility has been limited so far, although it
has shown promising results86.
Discussion
In the light of the review regarding the history of hy-
perbaric chambers and the use of hyperbaric oxygen
with therapeutic purposes, it can be suggested that the
physical, physiological and pathophysiological bases
support its use in different morbid processes. Hyperbar-
ic medicine is a field of science that has not yet been
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O. Huchim, et al.: History of hyperbaric medicine
859
fully explored, and although its use in many particular
conditions is not supported by evidence from random-
ized, controlled clinical trials concluding that the benefit
of this treatment is significantly superior to others in
statistical terms, it is also true that the effectiveness of
its use in pathological processes involving hypoperfu-
sion, infection, ischemia or infarction, either acutely or
chronically, has not been scientifically ruled out.
The effectiveness of hyperbaric oxygen should, in our
opinion, be evaluated as a co-adjuvant therapy in the
treatment of people with pathologies involving hypoper-
fusion, infection, ischemia or infarction processes, re-
gardless of the etiological nature that has generated said
morbid state, since if its effectiveness is tried to be as-
sessed disease by disease, this type of therapy will end
up being unnecessarily underused, since, if properly
used, it can allow patients healing in shorter time, having
less sequels or recovering aspects as important as sen-
sitivity or function, which will directly impact on patients’
quality of life, socialization and productivity.
An aspect that potentially can underlie hyperbaric
oxygen therapy underuse in different settings is the
cost it implies for insurance companies, which limit
their right-holders access to hyperbaric oxygen ther-
apy arguing the lack of evidence of its effectiveness
for the specific condition of each insured. A possible
solution to this conflict of interests might arise if
hyperbaric oxygen therapy indications were not spe-
cific for a disease, but for syndromes and pathological
processes involving hypoxia, hypoperfusion, infection,
ischemia or infarction; this way, the benefits of this
therapy could be offered to patients meeting these
criteria. This could even be considered an extra ben-
efit that would position insurance companies in advan-
tage over competitors, by offering therapies their com-
petition usually refuses.
Conclusion
As medical science advances, our knowledge re-
garding hyperbaric oxygen therapy will with no doubt
grow, and this is why hyperbaric medicine remains a
niche for clinical practice and research, which at
350 years of its initiation maintains the interest of
contemporary medical researchers who are looking to
improve the quality of life of their patients.
Conflicts of interests
The authors of the present work have no commer-
cial links or conflicts of interests to declare.
References
1. Edwards ML. Hyperbaric oxygen therapy. Part 1: history and principles.
J Vet Emerg Crit Care. 2010;20:284-8.
2. Shahriari A, Khooshideh M, Heidari M. Diseases treated with hyperbaric
oxygen therapy; a literature review. Med Hypothesis. 2014;1(1).
3. Hampson NB. Hyperbaric oxygen therapy: 2003 Committee Report. Un-
dersea and Hyperbaric Medical Society; 1999.
4. Gill A, Bell CN. Hyperbaric oxygen: its uses, mechanisms of action and
outcomes. QJM. 2004;97:385-95.
5. Boyle R. LXXXII. The solubility of radium emanation. Application of
Henry’s law at low partial pressures. The London, Edinburgh, and Dublin
Philosophical Magazine and Journal of Science. 1911;22:840-54.
6. Hulst RA, Klein J, Lachmann B. Gas embolism: pathophysiology and
treatment. Clin Physiol Funct Imaging. 2003;23:237-46.
7. Bouck GR. Etiology of gas bubble disease. Transactions of the American
Fisheries Society. 1980;109:703-7.
8. Tibbles PM, Edelsberg JS. Hyperbaric-oxygen therapy. N Engl J Med.
1996;334:1642-8.
9. Gabb G, Robin ED. Hyperbaric oxygen. A therapy in search of diseases.
Chest. 1987;92:1074-82.
10. Leach R, Rees P, Wilmshurst P. Hyperbaric oxygen therapy. BMJ.
1998;317:1140-3.
11. Balestra C, Germonpré P, Poortmans JR, et al. Serum erythropoietin levels
in healthy humans after a short period of normobaric and hyperbaric oxygen
breathing: the “normobaric oxygen paradox”. J Appl Physiol. 2006;100:512-8.
12. Boyle R, Kesaris P, Hunter MCW. Letters and papers of Robert Boyle:
a guide to the manuscripts and microfilm. Greenwood Pub Group; 1992.
13. Boyle R. The general history of the air London. Printed for Awnsham and
John Churchill; 1692.
14. Dalton J. On the constitution of mixed gases, on the force of steam of vapour
from water and other liquids in different temperatures, both in a Torricellia
vacuum and in air; on evaporation; and on the expansion of gases by heat.
Memoirs, Literary and Philosophical Society of Manchester. 1802;5:536-602.
15. Brown DR, Davis NL, Lepawsky M, et al. A multicenter review of the
treatment of major truncal necrotizing infections with and without hyper-
baric oxygen therapy. Am J Surg. 1994;167:485-9.
16. Clark L, Moon R. Hyperbaric oxygen in the treatment of life-threatening
soft-tissue infections. Respir Care Clin N Am. 1999;5:203-19.
17. Korhonen K, editor. Hyperbaric oxygen therapy in acute necrotizing in-
fections. With a special reference to the effects on tissue gas tensions.
Ann Chir Gynaecol. 2000;89(Suppl 214):7-36.
18. Borriello G, Werner E, Roe F, et al. Oxygen limitation contributes to
antibiotic tolerance of Pseudomonas aeruginosa in biofilms. Antimicrob
Agents Chemother. 2004;48:2659-64.
19. Myers RA. Hyperbaric oxygen therapy for trauma: crush injury, compart-
ment syndrome, and other acute traumatic peripheral ischemias. Int
Anesthesiol Clin. 2000;38:139-51.
20. Zamboni WA, Roth AC, Russell RC, et al. Morphologic analysis of the
microcirculation during reperfusion of ischemic skeletal muscle and the
effect of hyperbaric oxygen. Plast Reconstr Surg. 1993;91:1110-23.
21. Isik A, Peker K, Gursul C, et al. The effect of ozone and naringin on
intestinal ischemia/reperfusion injury in an experimental model. Int J
Surg. 2015;21:38-44.
22. Daniel RA, Cardoso VK, Góis Jr E, et al. Evaluation of pulmonary reper-
fusion injury in rats undergoing mesenteric ischemia and reperfusion and
protective effect of postconditioning on this process. Rev Bras Cir Car-
diovasc. 2015;30:533-7.
23. Andreadou I, Iliodromitis EK, Rassaf T, et al. The role of gasotransmitters
NO, H2S and CO in myocardial ischaemia/reperfusion injury and cardi-
oprotection by preconditioning, postconditioning and remote conditioning.
Br J Pharmacol. 2015;172:1587-606.
24. Neuman TS, Thom SR. Physiology and medicine of hyperbaric oxygen
therapy. Philadelphia: Saunders/Elsevier; 2008.
25. Aug G-B. Le mecanisme Cartesien et la physiologie au XVIIe siecle. Isis.
1914;2:37-89.
26. Manley G. The weather and diseases: some eighteenth-century contri-
butions to observational meteorology. Notes and Records of the Royal
Society of London. 1952;9:300-7.
27. Brimblecombe P. Air pollution in industrializing england. Journal of the
Air Pollution Control Association. 1978;28:115-8.
28. Arbuthnot J. An essay concerning the effects of air on human bodies: J.
Tonson; 1733.
29. Sprat T. The history of the Royal Society of London: for the improving
of natural knowledge. J. Knapton; 1734.
30. Henshaw N. Aërochalinos. London: editor desconocido; 1667.
31. Sternbach GL, Varon J. The discovery and rediscovery of oxygen. Emerg
Med J. 2005;28:221-4.
32. Williams CT. Aero-therapeutics or, the treatment of lung diseases by
climate; Being the Lumleian Lectures for 1893 delivered before the
Royal College of Physicians, with an address on the High Altitudes of
Colorado. Macmillan and Company; 1894.
No part of this publication may be reproduced or photocopying without the prior written permission of the publisher. © Permanyer 2018
Gaceta Médica de México. 2017;153
860
33. Djerassi C, Hoffmann R. From oxygen: a play in two acts. The Kenyon
Review. 2001;23:221-36.
34. Priestley J. The discovery of oxygen. Part 1: experiments. WF Clay;
1894.
35. Bowden ME, Rosner L. Joseph Priestley, radical thinker: a catalogue to
accompany the exhibit at the Chemical Heritage Foundation Commem-
orating the 200th anniversary of the death of Joseph Priestley. Chemical
Heritage Foundation; 2005.
36. Riera i Tuèbols S. La teoria del flogist, la química pneumàtica i Antoine
Laurent Lavoisier. Ciència 2a època. 2014;50:36-42.
37. Bert P, Hitchcock MA, Hitchcock FA. Barometric pressure. College Book
Company; 1943.
38. Davies JV. The tunnel construction of the Hudson and Manhattan
Railroad Company. Proc Am Philos Soc. 1910;49:164-87.
39. Smith AH. The effects of high atmospheric pressure: including the cais-
son disease. Eagle Book and Job Print; 1873. 53 p.
40. Butler W. Caisson disease during the construction of the Eads and
Brooklyn Bridges: a review. Undersea Hyperb Med. 2004 Win-
ter;31:445-59.
41. McCullough D. The Great Bridge: the epic story of the building of the
Brooklyn Bridge. Nueva York: Simon and Schuster; 2012. 605 p.
42. Vernon H. The solubility of air in fats, and its relation to caisson disease.
Proceedings of the Royal Society of London Series B, Containing Papers
of a Biological Character. 1907;79:366-71.
43. Boycoh A, Damant G. Experiments on the influence of fatness on sus-
ceptibility to caisson disease. J Hygiene. 1908;8:445-56. Erdmann W,
Bruley DF. Oxygen transport to jssue XIV. Springer US; 2012.
44. Aldrich C. Compressed-air illness, caisson disease. Int Clin. 1900;
10:73-88.
45. Boycott A, Haldane J. The effects of low atmospheric pressures on
respiration. J Physiol. 1908;37:355.
46. Thomson WA. The physiology of deep-sea diving. BMJ. 1935;2:208.
47. Gordon J, Heacock C. Roentgenologic demonstration of localized gas in
caisson disease. JAMA. 1940;114:570-1.
48. Powers JG, Higham C, Broussard K, et al. Wound healing and treating
wounds: chronic wound care and management. JAAD. 2016;74:607-25.
49. Feldmeier J, Hopf H, Warriner III R, et al. UHMS position statement:
topical oxygen for chronic wounds. Undersea Hyperb Med. 2005;32:157.
50. Bishop AJ. Diabetic lower extremity ulcers and hyperbaric oxygen ther-
apy. J Endocrinol Diab. 2015;2:1-5.
51. Stoekenbroek R, Santema T, Legemate D, et al. Hyperbaric oxygen for
the treatment of diabetic foot ulcers: a systematic review. Eur J Vasc
Endovasc Surg. 2014;47:647-55.
52. Fagher K, Katzman P, Löndahl M. Hyperbaric oxygen therapy reduces
the risk of QTc interval prolongation in patients with diabetes and hard-
to-heal foot ulcers. J Diabet Complications. 2015;29:1198-202.
53. Doctor N, Pandya S, Supe A. Hyperbaric oxygen therapy in diabetic foot.
J Postgrad Med. 1992;38:112.
54. Elraiyah T, Tsapas A, Prutsky G, et al. A systematic review and me-
ta-analysis of adjunctive therapies in diabetic foot ulcers. J Vasc Surg
Cases. 2016;63:46S-58S. e2.
55. Murphy-Lavoie H, Butler F, Hagan C. Central retinal artery occlusion
treated with oxygen: a literature review and treatment algorithm. Under-
sea Hyperb Med. 2012;39:943.
56. Vingolo EM, Rocco M, Grenga P, et al. Slowing the degenerative pro-
cess, long lasting effect of hyperbaric oxygen therapy in retinitis pigmen-
tosa. Graefes Arch Clin Exp Ophthalmol. 2008;246:93-8.
57. Körpinar Ş, Alkan Z, Yiğit Ö, et al. Factors influencing the outcome of
idiopathic sudden sensorineural hearing loss treated with hyperbaric
oxygen therapy. Eur Arch Otorhinolaryngol. 2011;268:41-7.
58. Holy R, Navara M, Dosel P, et al. Hyperbaric oxygen therapy in idiopath-
ic sudden sensorineural hearing loss (ISSNHL) in association with com-
bined treatment. Undersea Hyperb Med. 2011;38:137.
59. Plein CT, Harounian J, Floyd E, et al. A systematic review of eligibility
and outcomes in tinnitus trials reassessment of tinnitus guideline. Oto-
laryngol Head Neck Surg. 2016;154:24-32.
60. Cavallazzi G, Pignataro L, Capaccio P, editores. Italian experience in
hyperbaric oxygen therapy for idiopathic sudden sensorineural hearing
loss. International Joint Meeting on Hyperbaric and Underwater Medicine;
1996.
61. Stachler RJ, Chandrasekhar SS, Archer SM, et al. Clinical practice
guideline sudden hearing loss. Otolaryngol Head Neck Surg.
2012;146(3 Suppl):S1-S35.
62. Mukherjee A, Raison M, Sahni T, et al. Intensive rehabilitation combined
with HBO2 therapy in children with cerebral palsy: a controlled longitu-
dinal study. Undersea Hyperb Med. 2014;41:77-85.
63. Chen S-Y, Huang E, Wang V, et al. Improvement of clinical outcome and
cerebral perfusion in a patient of atherosclerotic cerebral infarction after
repetitive hyperbaric oxygen treatment – a case report and literature
review. Undersea Hyperb Med. 2011;38:375.
64. Shen M, He J, Cai J, et al. Hydrogen as a novel and effective treatment
of acute carbon monoxide poisoning. Med Hypotheses. 2010;75:235-7.
65. Valadão J, Pearl J, Verma S, et al. Hyperbaric oxygen treatment for
post-radiation central nervous system injury: a retrospective case series.
Undersea Hyperb Med. 2014;41:87-96.
66. Weaver LK, Valentine KJ, Hopkins RO. Carbon monoxide poisoning: risk
factors for cognitive sequelae and the role of hyperbaric oxygen. Am J
Respir Crit Care Med. 2007;176:491-7.
67. Peng Z, Wang S, Huang X, et al. Effect of hyperbaric oxygen therapy on
patients with herpes zoster. Undersea Hyperb Med. 2012;39:1083.
68. Freiberger JJ, Padilla-Burgos R, Chhoeu AH, et al. Hyperbaric oxygen
treatment and bisphosphonate-induced osteonecrosis of the jaw: a case
series. Oral Maxillofac Surg. 2007;65:1321-7.
69. Bent S, Bertoglio K, Ashwood P, et al. Brief report: hyperbaric oxygen
therapy (HBOT) in children with autism spectrum disorder: a clinical trial.
J Autism Dev Disord. 2012;42:1127-32.
70. Al-Waili NS, Butler GJ, Beale J, et al. Hyperbaric oxygen and malignan-
cies: a potential role in radiotherapy, chemotherapy, tumor surgery and
phototherapy. Med Sci Monit. 2005;11:RA279-RA289.
71. Fredman R, Wise I, Friedman T, et al. Skin-sparing mastectomy flap
ischemia salvage using urgent hyperbaric chamber oxygen therapy: a
case report. Undersea Hyperb Med. 2014;41:145-7.
72. Thom SR. Hyperbaric oxygen – its mechanisms and efficacy. Plast Re-
constr Surg. 2011;127(Suppl 1):131S.
73. Khandelwal S, Wall J, Kaide C, et al. Case report: successful use of
hyperbaric oxygen therapy for a complete scalp degloving injury. Under-
sea Hyperb Med. 2008;35:441-5.
74. Chong KT, Hampson NB, Corman JM. Early hyperbaric oxygen therapy
improves outcome for radiation-induced hemorrhagic cystitis. Urology.
2005;65:649-53.
75. Hassan Z, Mullins RF, Friedman BC, et al. Treating necrotizing fasciitis with
or without hyperbaric oxygen therapy. Undersea Hyperb Med. 2010;37:115.
76. Mortensen CR. Hyperbaric oxygen therapy. Curr Anaesth Crit Care.
2008;19:333-7.
77. Bakker DJ. Clostridial myonecrosis (gas gangrene). Undersea Hyperb
Med. 2012;39:731.
78. Jordan JE, Zhao ZQ, Vinten-Johansen J. The role of neutrophils in
myocardial ischemia-reperfusion injury. Cardiovasc Res. 1999;43:860-78.
79. Weyker PD, Webb CA, Kiamanesh D, et al. Lung ischemia reperfusion
injury: a bench-to-bedside review. Semin Cardiothorac Vasc Anesth.
2013;17:28-43.
80. Yu WK, Chen YW, Shie HG, et al. Hyperbaric oxygen therapy as an
adjunctive treatment for sternal infection and osteomyelitis after sternot-
omy and cardiothoracic surgery. J Cardiothorac Surg. 2011;6:1.
81. McGrath T, Hamilton R. Hyperbaric oxygen in the treatment of venomous
snake bites. Undersea Hyperb Med. 2010;37:393-4.
82. Quinn DK, McGahee SM, Politte LC, et al. Complications of carbon
monoxide poisoning: a case discussion and review of the literature. Prim
Care Companion J Clin Psychiatry. 2009;11:74-9.
83. Cooper JS, Allinson P, Keim L, et al. Hyperbaric oxygen: a useful adjunct
for purpura fulminans: case report and review of the literature. Undersea
Hyperb Med. 2014;41:51-7.
84. Graffeo C, Dishong W. Severe blood loss anemia in a Jehovah’s Witness
treated with adjunctive hyperbaric oxygen therapy. Am J Emerg Med.
2013;31:756. e3-4.
85. Hart G, Lennon P, Strauss M. Hyperbaric oxygen in exceptional acute
blood-loss anemia. Undersea Hyperb Med. 1987;2:205-10.
86. Pineda JF, Ortiz CG, Miguel G de J, et al. Improvement in serum an-
ti-Müllerian hormone levels in infertile patients after hyperbaric oxygen
(preliminary results). JBRA Assisted Reproduction. 2015;19:87-90.
No part of this publication may be reproduced or photocopying without the prior written permission of the publisher. © Permanyer 2018
