Comprehensive information about diving and undersea medicine for the non-medical diver, the non-diving physician and the specialist.
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Comprehensive information about diving and undersea medicine for the non-medical diver, the non-diving physician and the specialist. |
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Hyperbaric Oxygen Therapy
Hyperbaric Oxygen Therapy
(JAMA Article)
Subjects
Hyperbaric oxygenation Evaluation
Oxygen therapy Complications
Hyperbaric oxygenation Complications
Reference #: A8988013
Abstract
Hyperbaric oxygen (HBO) therapy involves intermittent inhalation of pure oxygen under a pressure greater than one atmosphere.
During the 1960s, HBO was proposed as a treatment for cancer, heart attack, senility, and other conditions, but research studies did not obtain reproducible results. The skepticism engendered among medical personnel by these failures extended to HBO's use for treating clinical conditions that it had been shown to help. A review of these conditions is provided. HBO acts both mechanically, due to its pressure component, and physiologically, due to its oxygen component.
HBO therapy has been effective in treating decompression sickness (the illness resulting from too-rapid changes in pressure by divers or aviators), and air embolism (introduction of air into the circulatory system, often unintentionally by medical personnel) by mechanically reducing the size of gas bubbles, and increasing oxygen levels in the blood.
Oxygen is essential for proper function of certain cells of the immune system and, in certain injuries, such as burns and crush injuries, HBO treatment can increase the supply of oxygen to tissues otherwise deprived of it. Complications of HBO treatment include trauma to or rupture of cavities, neurotoxicity resulting from exposure to 100 percent oxygen for long periods, and other sequelae.
HBO therapy is indicated for decompression sickness, air embolism, carbon monoxide poisoning, acute traumatic ischemia (crush injuries that deprive tissues of oxygen), and bacterial invasion of a necrotic wound (in which tissue has died). HBO may also stimulate regrowth of blood vessels in damaged tissue adjacent to areas treated by radiation therapy and may promote bone formation in cases of osteomyelitis (bone infection) that have not responded to other treatments. This therapy also shows promise for treating a variety of 'problem wounds', but randomized, prospective studies are lacking.
Overall, HBO therapy is safe and effective for certain conditions, and well-formulated clinical trials could help extend its use to others. (Consumer Summary produced by Reliance Medical Information, Inc.)
=================================================================
Full Text
Copyright American Medical
Association
1990
HYPERBARIC OXYGEN THERAPY
Hyperbaric oxygen
therapy
involves intermittent inhalation of
100% oxygen under a pressure
greater than 1 atm. Despite over a
century of use in
medical settings, hyperbaric oxygen remains a
controversial therapy.
The last 20 years
have
seen a clarification of the mechanism of
action of hyperbaric therapy
and a greater understanding of its
potential benefit. However,
despite the substantial evidence that
hyperbaric oxygen
may have a therapeutic effect in certain
carefully defined
disease states, many practitioners remain
unaware of these findings or
are concerned about using hyperbaric
therapy because of the
controversy
it has engendered. This review
examines the
indications
currently considered appropriate for
hyperbaric oxygen and briefly
evaluates animal and clinical data
substantiating these
indications.
Areas in which the mechanism of
action of hyperbaric oxygen
is still not well understood, as well
as possible new areas of
applications,
are discussed.
HYPERBARIC oxygen
(HBO)
therapy involves intermittent inhalation
of 100% oxygen under a
pressure
greater than 1 atm. [1]
Both therapeutic and
toxic
effects result from two features of
treatment: mechanical effects
of increased pressure and
physiologic effects of
hyperoxia.
Hyperbaric
oxygen
therapy has long been accepted as a primary
treatment for decompression
sickness [2]; however, other proposed
indications have been
controversial.
During the 1960s there was
widespread enthusiasm
for hyperbaric treatment of myocardial
infarction, stroke,
senility,
and cancer. Enthusiasm waned after
results of clinical
trials
(and direct experience) showed little
benefit for these
diseases.
The overzealous claims about the
effectiveness of
HBO therapy have left a legacy of skepticism
among physicians. [3]
However, animal studies, clinical trials,
and greater clinical
experience
over the last two decades have
produced a
set
of indications for which HBO therapy appears
beneficial. These clinical
conditions
are substantially different
from those in
the
1960s. However, there has been no recent
interdisciplinary review of
HBO therapy delineating these current
indications, despite their
broad
applications.
Thus, while substantial
evidence
supports use of HBO therapy in
certain carefully
de fined settings, many patients who might
benefit go untreated
because
of their physician's unfamilarity
with recent research and
overall
uncertainty about the legitimacy
of HBO as therapy. We discuss
the mechanism of action of HBO
therapy and the commonly
accepted clinical indications (Table 1)
as delineated by the Undersea
and Hyperbaric Medical Society, [1]
the professional
association of physicians administering HBO
therapy, and we
briefly review the data supporting current
indications.
MECHANISMS OF ACTION
Pressure
In disease such
as air embolism and decompression sickness, the
therapeutic effect
of HBO therapy is achieved through
the
mechanical reduction in bubble
size brought on by an increase in
ambient pressure. A 5 atm a
bubble is reduced to 20% of its
original volume and 60% of its
original diameter.
Increasing
pressure
in HBO therapy is often expressed in
multiples of atmospheric
pressure
absolute (ATA); 1 ATA equals 1
kg/c[m.sup.2] or 735.5 mm Hg.
Most HBO treatments are performed
at 2 to 3 ATA. In air
embolism and decompression sickness, where
pressure is crucial to
therapeutic effect, treatments frequently
start at 6 ATA.
This additional pressure,
when
associated with inspiration of
high levels
of
oxygen, substantially increases the level of
oxygen dissolved into blood
plasma. This state of serum hyperoxia
is the second beneficial
effect
of hyperbaric oxygen therapy.
Hyperoxia: Life Without
Blood
At sea level
in room air, hemoglobin is approximately
97%
saturated with oxygen (19.5
vol% oxygen, of which approximately
5.8 vol% is extracted
by tissue). The amount of oxygen dissolved
into plasma is
0.32
vol%. An increase in P[O.sub.2] has a
negligible impact on total
hemoglobin
oxygen content; however, it
does result in an
increase
in the amount of oxygen dissolve
directly into
plasma.
With 100% inspired oxygen the amount of
plasma oxygen increases
to
2.09 vol%. At 3 ATA plasma contains
6.8 vol% oxygen,
a level equivalent to the average
tissue
requirements for
oxygen. Thus, HBO treatment could and has
sustained life without
hemoglobin.
[4]
The immune
system,
wound healing, and vascular tone are all
affected by
oxygen
supply. Oxygen alone has little direct
antimicrobial
effect,
even for most anaerobes [5]; it is,
however, a crucial factor in
immune function.
Neutrophils require
molecular
oxygen as a substrate for microbial
killing. The
oxidative
burst seen in
neutrophils
after
phagocytosis of
bacteria involves a 10-to 15-fold increase in
oxygen consumption. [6] Here
oxygen serves as a substrate in the
formation of free radicals,
which directly or indirectly initiate
phagocytic killing. [7] This
endogenous antimicrobial system
virtually ceases
functioning under conditions of hypoxia. A
tissue [PO.sub.2] of at
least
30 mm Hg of oxygen is considered
necessary for normal
oxidative
function to occur. [8] Oxygen
partial pressures
below this are often seen in damaged and
infected tissues. Increasing
the oxygen level in this tissue can
allow restoration of white
blood
cell function and return of
adequate antimicrobial
action. [9] The cardiovascular effects of
hyperbaric oxygen
include
a generalized vasoconstriction and a
small reduction in
cardiac
output. [10] This ultimately may
decrease the
overall
blood supply to a region, but the increase
in serum oxygen content
results
in an overall gain in delivered
oxygen. In conditions such as
burns, cerebral edema, and crush
injuries, this
vasoconstriction
may be beneficial, reducing edema
and tissue swelling while main
taining tissue oxygenation. [11]
COMPLICATIONS
Usual
complications
of HBO therapy are listed in Table 2. They
are a result of
either barometric pressure changes or oxygen
toxicity. The most common
complications
involve cavity trauma due
to change in pressure. [12]
Any air-filled cavity that cannot
equilibrate with
ambient pressure, such as the middle ear when
the eustachian
tube
is blocked, is subject to deformity and
barotrauma during pressure
changes
in HBO therapy.
Pneumothorax is a
rare
complication of HBO treatment,
usually occurring only in
patients
with severe lung disease.
Air embolism,
presumably
resulting from a small tear in
the pulmonary vasculature, is
another rare complication. [13] One
hundred percent oxygen under
high pressure is neurotoxic and can
lower the seizure threshold
and affect central nervous system
control of
respiration.
However, neurotoxicity is rare with the
low-pressure,
short-duration
treatments used clinically in HBO
therapy. In one series the
incidence
was reported as 1.3 seizures
per 10 000 treatments. [14]
Pulmonary oxygen toxic
reactions
can occur with 100% inspired
oxygen at
less
than 1 ATA with prolonged exposure. Almost all
patients will show pulmonary
toxicity after 6 continuous hours of
inspired oxygen at 2
ATA.
[15] No clinical HBO protocol requires
this length of continuous
exposure
to 100% oxygen. However, HBO
treatments may
contribute
to the pulmonary oxygen toxicity seen
in critically ill
patients
who receive high concentrations of
inspired oxygen between
hyperbaric
treatments.
Although a concern in
premature
newborns, retrolental fibroplasia
has not been noted in infants,
children, or adults undergoing HBO
therapy. [16]
Development
of cataracts has been reported in
patients receiving more than
150 HBO treatments. [17]
HBO ADMINISTRATION
Hyperbaric oxygen can be
administered
in either a multiplace or a
monoplace chamber.
Multiplace Chamber
Multiplace chambers
are
large tanks accommodating 2 to 14 people
(Fig 1). They are usually
built
to achieve pressures up to 6 atm
and have a chamber lock-entry
system that allows personnel to
pass through without
altering
the pressure of the inner chamber.
Patients can be directly
cared for by medical staff within the
chamber. The chamber is
filled with compressed air; patients
breathe
100%
oxygen through a face mask, head
hood,
or
endotracheal tube.
Although
fire hazards restrict the use of
certain electronic equipment,
some monitors and ventilators with
solid-state
circuitry
can be used within the chamber, allowing
intensive care of
critically
ill patients. [18] The multiplace
chamber's ability to maintain
pressures of 6 atm or more, makes
it the
chamber
of choice for decompression sickness and air
embolism.
Monoplace Chamber
Monoplace chambers (Fig 2)
are
far less costly than their larger
counterparts and have allowed
hospitals to institute HBO programs
without prohibitive capital
outlays. Most chambers are sized to
allow a single patient
to lie supine under a transparent acrylic
dome or viewing
port.
The internal environment of a monoplace
chamber is maintained at 100%
oxygen; thus, the patient does not
wear a mask. This high
concentration of oxygen precludes the use
of any electronic
equipment
in the chamber. However, specially
adapted ventilators and
monitoring
systems do allow treatment of
critically ill patients.
CLINICAL INDICATIONS
Acute Conditions
Decompression Sickness:
Although occasionally seen in
aviators, decompression sickness is
generally a
disease
of divers. During a dive, the diver is
exposed to pressures
greater
than 1 atm, and tissue uptake of
nitrogen increases according
to the principles of Henry's law.
With ascent,
a
pressure gradient develops, and nitrogen leaves
the tissue, dissolving into
the blood and passing to the lungs,
where it is exhaled. With
rapid
ascent a steep pressure gradient
develops and
intravascular
nitrogen gas bubbles form. [19] These
can be
detected
in asymptomatic divers. [20] With greater
pressure gradients, the
nitrogen
bubbles become large enough and
prevalent enough to
mechanically
deform tissue and obstruct blood
vessels. The gas-fluid
interface
also interacts with blood cells,
platelets, and proteins,
causing
disruption of the intravascular
coagulation system. [21]
Decompression
sickness results.
Divers can
experience
decompression sickness as pain only,
usually as a
"deep and dull ache" in the extremities. More
serious cases
can
present as paraplegia or cardiovascular
collapse due to
embolization
of bubbles into the cardiac or
central nervous system.
Hyperbaric oxygen
therapy
mechanically decreases the size of the
bubbles, oxygenates
ischemic
tissue, and reduces the nitrogen
gradient. Any
patient
with decompression sickness should be
transferred
immediately
to the nearest HBO facility with the
capacity to decompress to 3
to 6 ATA, as this has been shown in
numerous series to be the most
reliable and effective treatment.
[22,23] The
Duke
University Divers Alert Network maintains a
24-hour emergency
consultation
telephone number, (919) 684-9111,
and can identify the closest
available HBO facility.
Air Embolism.
Air embolism can be a
complication
of uncontrolled ascent in
diving but
more
frequently is seen medically in iatrogenic
misadventures. Bubbles
can
embolize to the cerebral or cardiac
circulation,
producing
either severe neurologic symptoms or
sudden death.
Hyperbaric
oxygen therapy has been part of
successful
treatment
of air embolism due to cardiovascular
procedures,
[24,25]
lung biopsies, [26] hemodialysis, [27] and
central line placement.
[28] Presumably, HBO therapy decreases
the volume of the embolism and
oxygenates local tissues.
Treatment involves
immediate
descent to 6 ATA for 15 to 30
minutes on air,
followed by decompression to 2.8 ATA, where the
patient receives
prolonged oxygen treatment. Carbon Monoxide
Poisoning.—Carbon monoxide
poisoning
accounts for half of all
fatal poisonings in the United
States. Multiple series have shown
that patients
with
carbon monoxide poisoning improve markedly
following treatment with HBO.
[29-31] However, both the mechanism
of carbon monoxide toxicity
and the therapeutic effect of HBO are
poorly understood. Carbon
monoxide
toxicity was long thought to
be due to anoxia alone; [32]
however, there is evidence that the
pathophysiologic
effects
occur with carbon monoxide binding to
the
cytochrome-oxidase
system, causing anoxia
at
the
mitochondrial level. [33] In
either case, HBO therapy is the most
rapid way of displacing carbon
monoxide bound to hemoglobin and
cytochromes.
The
serum half-life of carboxyhemoglobin is
decreased from 5 hours
20 minutes with room air to 80 minutes
with 100% oxygen and 23
minutes
with 100% oxygen at 3 ATA. [34]
In treating
patients
with carbon monoxide poisoning, it is
important to remember that
serum
carboxyhemoglobin levels do no t
reflect tissue levels
of carboxyhemoglobin and, therefore, may
not correlate with the degree
of toxicity. Accompanying signs and
symptoms are as
important to guiding therapy as the
serum
carboxyhemoglobin
level.
[35] Although HBO therapy remains the
preferred treatment for
significant exposure (Table 3), only a
few controlled
human
studies with inconclusive results have
compared HBO with 100% oxygen
at 1 atm. [36,37]
Clostridial Myonecrosis.
Clostridial
myonecrosis
occurs when a hypoxic environment within
a necrotic
wound
allows clostridial spores to
convert
to
vegetative organisms.
These organisms produce exotoxins that
destroy red blood cells, cause
tissue necrosis, and abolish local
host defenses.
The
most important exotoxin is alpha toxin. A
tissue [PO.sub.2] of 250
mm
Hg inhibits the production of alpha
toxin by Clostridium. [38]
Hyperbaric oxygen is
commonly
used as an adjunct therapy in
clostridial
infections.
In vivo studies have demonstrated
decreased mortality rates
and
diminished tissue loss in infected
mice. [39,40] In a study by
DeMello et al, [41] using a dog model
of clinical Clostridium
infection,
100% of infected control dogs
and dogs randomized to
either HBO therapy or surgery died. Fifty
percent of the dogs
that
received antibiotics survived, 70% of
the dogs
that
received antibiotics and underwent
surgery
survived, and 95%
of the dogs that received antibiotics and HBO
therapy and underwent surgery
survived.
Multiple series
have
evaluated the effect of HBO therapy on
clostridial infections in
humans.
[42,43] Surgeons experienced
with its use emphasize
that early HBO treatment reduces systemic
toxic reactions so that
patients in shock seem more stable and
better able to tolerate
surgery,
and there is clearer demarcation
of viable and nonviable
tissue.
There have, however, been no
randomized, controlled studies.
Hyperbaric
oxygen
therapy has been recommended for treatment of
necrotizing fasciitis,
since
anaerobic bacteria play a role in
the disease.
[44,45]
The diversity of clinical states in
retrospective
studies
and the paucity of experimental data make
it difficult
to
demonstrate the effect of HBO
therapy
on
nonclostridial
soft-tissue
infection. Although necrotizing
fasciitis is an accepted
indication
for HBO, the benefit HBO
therapy may
provide
is still poorly understood, and surgery
remains the cornerstone of
therapy.
[46]
Acute Traumatic
Ischemia.
Acute crush injury to
an extremity may cause severe edema and
ischemia in tissue and
capillary
beds not relieved by restoration
of arterial perfusion.
Hyperbaric
oxygen therapy may aid salvage
during the
acute
stages of revascularization by reducing edema
via vasoconstriction and
increasing oxygen delivery via plasma
flow. [47] Investigators have
used HBO therapy successfully as an
adjunct to surgery in crush
injuries. [48,49] Additional evidence
has demonstrate d that HBO
therapy
may also serve as an adjunct
therapy in the compartment
syndrome.
[50]
CHRONIC CONDITIONS
Irradiated Tissue.
Radiation therapy,
in addition to its therapeutic effects, can
damage normal adjacent
tissue.
The initial pathologic process is
a progressive obliterative
endarteritis,
resulting in areas of
tissue hypoxia
and
eventual cell death. [51] Large areas of
hypocellular, hypovascular,
and hypoxic tissue are created that
are devoid of functioning
fibroblasts
and osteoblasts. [52]
Hyperbaric oxygen therapy
appears
to assist in salvaging such
tissue by
stimulating angioneogenesis in marginally viable
tissue. [53]
Marx
and Johnson [54] emphasize
that,
in
reconstructive
surgery
involving recently irradiated tissue,
presurgical HBO treatment can
help promote a well-vascularized
wound bed that will
enhance
reconstruction and graft take. Using
a specific
HBO
protocol of presurgical and
postsurgical
treatments, they demonstrated
a satisfactory surgical outcome in
92% of their patients and a
complication rate of 9%.
In osteoradionecrosis,
tissue
destruction progresses to breakdown
of overlying
tissues
and symptomatic destruction of bone. Prior
to the introduction of
HBO
therapy, only 5% to 30% of patients
who developed
osteoradionecrosis
could expect remission with
conservative therapy.
[55] In a protocol developed by Marx, [56]
a series of
58
patients received an initial series of HBO
treatments, followed by
debridement
and further HBO treatment, as
dictated by their clinical
course.
All 58 patients studied had
resolution of
symptoms
of osteoradionecrosis, with good results
on long-term
follow
up. These impressive results have been
corroborated by others.
[57,58]
Successful results have also been
demonstrated for
radiation-induced cystitis [59] and other
radiation-damaged soft
tissue. [60] Hyperbaric oxygen therapy is
beneficial for
patients
at risk for the development of
osteoradionecrosis, such as
irradiated patients requiring tooth
extraction. In
a
randomized trial comparing HBO and penicillin
therapy in
74
pr eviously irradiated patients, 30% of
the
patients who received
penicillin developed osteoradionecrosis,
while
5.4%
of the patients who received
HBO developed
osteoradionecrosis.
[61]
Similar results have been reported
elsewhere. [62]
Refractory Osteomyelitis.
Hyperbaric oxygen
is currently being used as an adjunctive
therapy with debridement and
antibiotics in osteomyelitis that
has remained refractory
to standard therapy. Animal studies have
demonstrated that
HBO
therapy used in experimental models of
osteomyelitis has
increased
osseous repair [63] and promoted
callus formation, [64]
possibly
by promoting osteoclast activity.
[65] Human
studies
involve series of patients in whom standard
treatment
regimens
have failed. Multiple clinical
series
demonstrate
substantial
success with HBO therapy in these
patients. [66-68]
However,
to date there have been no randomized
trials.
Problem Wounds.
The rationale
for
HBO therapy in problem
wounds
is to
intermittently increase the
tissue oxygen tension to optimize
fibroblast
proliferation
[69] and white blood cell killing
capacity [70]
during
periods of hyperoxia and to stimulate
angioneogenesis during
periods
of relative hypoxia. [71] Series
have been published showing
improved healing with HBO therapy in
problem wounds
refractory
to standard therapy. [72,73] Patients
in whom increased
oxygenation of wounds can be demonstrated
following HBO therapy are the
most likely to benefit. However,
unlike
osteoradionecrosis,
where a well-defined clinical problem
has been shown to
improve with a carefully designed protocol
incorporating HBO therapy,
treatment
of problem wounds remains an
ill-defined field, and HBO
data
often consist of small series
without standardized patient
populations or treatment schedules.
Hyperbaric
oxygen
therapy cannot substitute for surgical
revascularization in
advanced
arterial insufficiency and cannot
reverse inadequate
microvascular
circulation. [74] Hyperbaric
oxygen therapy
may
serve as an adjunct in the treatment of
certain problem wounds,
but it cannot replace meticulous local
care based on sound
physiologic
principles.
Special Considerations
Certain animal data indicate
that HBO therapy may improve the
outcome of moderate and severe
burns. [75] Few centers use HBO as
standard therapy, but
recent publications of patient series have
demonstrated good
response.
[76-78] Broad-based justification of
the use of HBO in
burns, however, will depend on favorable
results of randomized clinical
trials.
SUMMARY
Hyperbaric oxygen therapy
is
a safe and effective primary therapy
when administered
for decompression sickness and air embolism.
The role of HBO as
an adjunctive therapy in the treatment and
prevention
of
osteoradionecrosis has been
impressively
documented. Its
contribution to the treatment of clostridial
myonecrosis has
been
substantiated by both animal models and
clinical experience. The role
of HBO therapy in recovery from
carbon monoxide
poisoning,
while probably significant, is poorly
understood and awaits
clarification
of the mechanism of action of
both carbon
monoxide
poisoning and the beneficial effects of
oxygen therapy.
Hyperbaric oxygen
therapy
is clearly of value for carefully
defined
indications.
Successful extension of its use in other
situations will
be predicated on in
vitro
and in vivo
experimental evidence
and
appropriate well-controlled clinical
trials.
References
[1.] Hyperbaric Oxygen
Therapy:
A Committee Report. Bethesda, Md:
Undersea and Hyperbaric
Medical
Society; 1986.
[2.] Francis
TJ,
Dutka AJ, Hallenbeck JM. Pathophysiology of
decompression
sickness.
In: Bove AA, Davis JC, eds. Diving
Medicine. Philadelphia, Pa:
WB Saunders Co; 1990:170-187.
[3.] Gabb G, Robin ED.
Hyperbaric
oxygen: a therapy in search of
diseases. Chest.
1987;92:1074-1082.
[4.] Boerema
I,
Meyne NG, Brummelkamp WK, et al. Life without
blood: a study of the
influence of high atmospheric pressure and
hypothermia
on
dilution of blood. J
Cardiovasc
Surg.
1960;1:133-146.
[5.] Tally
FP,
Stewart PR, Sutter VL, Rosenblatt JE. Oxygen
tolerance of fresh clinical
anaerobic bacteria. J Clin Microbiol.
1975;1:161-164.
[6.] Badwey JA,
Karnovsky
ML. Active oxygen species and the
functions
of
phagocytic leukocytes. Ann
Rev
Biochem.
1980;49:695-726.
[7.] Forman
HJ,
Thomas MJ. Oxidant production and bactericidal
activity of phagocytes. Ann
Rev Physiol. 1986;48:669-680.
[8.] Hohn DC,
MacKay
RD, Halliday B, Hunt TK. The effect of
[O.sub.2] tension on the
microbicidal
function of leukocytes in
wounds and in vitro. Surg
Forum.
1976;27:18-20.
[9.] Knighton
DR,
Halliday B, Hunt TK. Oxygen as an antibiotic:
the effect
of
inspired oxygen on infection.
Arch
Surg.
1984;119:199-204.
[10.] Risber J, Tyssebotn
I.
Hyperbaric exposure to a 5 ATA
He-[N.sub.2]-[O.sub.2]
atmosphere affects the cardiac function
and organ blood flow
distribution
in awake trained rats. Undersea
Biomed Res. 1986;13:77-90.
[11.] Nylander G, Lewis
D,
Nordstrom H, Larsson J. Reduction of
postischemic edema with
hyperbaric
oxygen. Plast Reconstr Surg.
1985;76:596-601.
[12.] Bassett
BE,
Bennett PB. Introduction to the physical and
physiological bases of
hyperbaric
therapy. In: Davis JC, Hunt TK,
eds. Hyperbaric
Oxygen Therapy. Bethesda, Md: Undersea and
Hyperbaric Medical Society;
1977:11-24.
[13.] Bond GF.
Arterial
gas embolism. In: Davis JC, Hunt, TK,
eds. Hyperbaric
Oxygen Therapy. Bethesda, Md: Undersea and
Hyperbaric Medical Society;
1977:141-152.
[14.] Davis JC,
Dunn
JM, Heimbach RD. Hyperbaric medicine:
patient selection,
treatment procedures, and side effects. In:
Davis JC, Hunt TK, eds.
Problem Wounds: The Role of Oxygen. New
York, NY: Elsevier Science
Publishing
Co Inc; 1988;225-235.
[15.] Clark JM,
Lambertson
CJ. Pulmonary oxygen toxicity: a
review. Pharmacol Rev.
1971;23:37-133.
[16.] Nichols CW,
Lambertsen
CJ. Effects of high oxygen pressures
on the eye. N Engl J Med.
1969;291:25-30.
[17.] Palmquist
BM,
Phillipson B, Barr PO. Nuclear cataract and
myopia during
hyperbaric
oxygen therapy. Br J Ophthalmol.
1984;68:113-117.
[18.] Kindwall
EP,
Goldman RW, eds.
Hyperbaric
Medical
Procedures. Milwaukee, Wis:
Saint Lukes Medical Center; 1988.
[19.] Lynch PR,
Brigham
M, Tuma R, Wiedeman MP. Origin and time
course of
gas
bubbles following rapid decompression in the
hamster. Undersea Biomed Res.
1985;12:105-114.
[20.] Whitecraft DD,
Karas
S. Air embolism and decompression
sickness in scuba divers.
JACEP.
1976;5:355-361.
[21.] Tanoue
K,
Mano Y, Kuroiwa K, Suzuki H, Shibayama M,
Yamazaki H. Consumption of
platelets
in decompression sickness of
rabbits. J Appl Physiol.
1987;62:1772-1779.
[22.] Kizer KW.
Delayed
treatment of dysbarism: a retrospective
review of 50 cases. JAMA.
1982;247:2555-2558.
[23.] Green RD, Leitch DR.
Twenty
years of treating decompression
sickness. Aviat Space Environ
Med. 1987;58:362-366.
[24.] Thomatis L, Nemiroff
M,
Riahi M, et al. Massive arterial
air
embolism
due to rupture of pulsatile assist
device:
successful treatment in
the
hyperbaric chamber. Ann Thorac Surg.
1981;32:604-608.
[25.] Peirce EC II.
Specific
therapy for arterial air embolism.
Ann Thorac Surg.
1980;29:300-303.
[26.] Cianci
P,
Posin JP, Shimshak RR, Singzon J. Air embolism
complicating
percutaneous
thin needle biopsy of lung. Chest.
1987;92:749-750.
[27.] Baskin
FE,
Wozniak RL. Hyperbaric oxygenation in the
treatment of
hemodialysis
associated air embolism. N Engl J Med.
1975;293:184-185.
[28.] Murphy BP,
Hartford
FJ, Cramer FS. Cerebral air embolism
resulting from
invasive
medical procedures: treatment with
hyperbaric oxygen. Ann Surg.
1985;201:242-245.
[29.] Myers
RAM,
Snyder SK, Linberg S, Cowley RA. Value of
hyperbaric oxygen in
suspected
carbon monoxide poisoning. JAMA.
1981;246:2478-2480.
[30.] Norkool DM,
Kirkpatrick
JN. Treatment of acute carbon
monoxide poisoning with
hyperbaric
oxygen: a review of 115 cases.
Ann Emerg Med.
1985;14:1168-1171.
[31.] Goldbaum LR,
Ramirez
RG, Absalom KB. What is the mechanism
of carbon
monoxide toxicity? Aviat
Space
Environ Med.
1975;46:1289-1291.
[32.] Jackson DL, Menges H.
Accidental
carbon monoxide poisoning.
JAMA. 1980;243:772-774.
[33.] Kindwall
EP.
Carbon monoxide poisoning treated with
hyperbaric oxygen. Respir
Ther.
1975;5:29-33.
[34.] Peterson
JE,
Stewart RD. Absorption and elimination of
carbon monoxide by
inactive young men. Arch Environ Health.
1970;21:165-175.
[35.] Kindwall EP. Carbon
monoxide
and cyanide poisoning. In:
Davis JC, Hunt TK,
eds. Problem Wounds: The Role of Oxygen. New
York, NY: Elsevier Science
Publishing
Co Inc; 1988:177-190.
[36.] Raphael JC,
Elkharrat
D, Jars-Guincestre MC, et al. Trial
of normobaric and hyperbaric
oxygen for acute carbon monoxide
intoxication. Lancet.
1989;2:414-419.
[37.] Goulon
M,
Barois A, Rapin M, Nouailhat F, Grosbuis S,
Labrousse J.
Carbon
monoxide poisoning and acute anoxia. J
Hyperbar Med. 1986;1:23-41.
[38.] Van
Unnik
AJM. Inhibition of toxin
production
in
Clostridium
perfringens
in vitro by hyperbaric oxygen. Antonie
von Leeuwenhoek.
1965;31:181-186.
[39.] Holland JA,
Hill
GB, Wolfe WG, Osterhout S, Saltzman HA,
Brown IW. Experimental and
clinical
experience with hyperbaric
oxygen in
the
treatment of clostridial myonecrosis. Surgery.
1975;77:75-85.
[40.] Hill GB,
Osterhout
S. Experimental effects of hyperbaric
oxygen on selected clostridial
species, II: in vivo studies in
mice. J Infect Dis.
1972;125:26-35.
[41.] DeMello
FJ,
Haglin JJ, Hitchcock CR. Comparative study of
experimental Clostridium
perfringens infection in dogs treated
with antibiotic,
surgery, and hyperbaric oxygen.
Surgery.
1973;73:936-941.
[42.] Gibson
A,
Davis FM. Hyperbaric oxygen therapy in the
management of
Clostridium
perfringens infections. N Z Med J.
1986;99:617-620.
[43.] Hart GB, Lamb RC,
Strauss
MB. Gas gangrene, II: a 15-year
experience with hyperbaric
oxygen.
J Trauma. 1983;23:995-1000.
[44.] Schreiner
A,
Tonjum S, Digranes A. Hyperbaric oxygen
therapy in Bacteroides
infections.
Acta Chir Scand. 1974;140:73-76.
[45.] Bakker DJ.
Necrotizing
soft tissue infections. J Hyperbar
Med. 1987;2:161-169.
[46.] Miller JD. The
importance
of early diagnosis and surgical
treatment
of
necrotizing faciitis. Surg Gynecol
Obstet.
1983;157:197-200.
[47.] Davis JC,
Heckman
JD. Compromised soft tissue wounds. In:
Davis JC, Hunt TK, eds.
Problem
Wounds: The Role of Oxygen. New
York, NY: Elsevier Science
Publishing
Co Inc; 1988:125-142.
[48.] Loder RE.
Hyperbaric
oxygen therapy in acute trauma. Ann R
Coll Surg Engl.
1979;61:472-473.
[49.] Monies-Chass I,
Hashmonai
M, Hoerer D, Kaufman T, Steiner
E, Schramek
A.
Hyperbaric oxygen treatment as an adjuvant to
reconstructive
vascular surgery
in
trauma. Injury.
1977;8:274-277.
[50.] Strauss MB,
Hargens
AR, Gershuni DH, et al. Reduction of
skeletal muscle necrosis
using intermittent hyperbaric oxygen in
a model
compartment
syndrome. J Bone Joint
Surg Am.
1983;65:656-662.
[51.] Ewing J.
Radiation
osteitis. Acta Radiol.
1926;6:399-412.
[52.] Marx
RE.
Osteoradionecrosis: s new concept
of
its
pathophysiology. J Oral
Maxillofac
Surg. 1983;41:283-288.
[53.] Hunt TK, Dai
MP.
The effect of varying ambient oxygen
tensions on wound metabolism
and collagen synthesis. Surg Gynecol
Obstet. 1972;135:561-567.
[54.]
Marx
RE, Johnson RP. Problem wounds
in
oral and
maxillofacial surgery: the
role
of hyperbaric oxygen. In: Davis JC,
Hunt TK, eds. Problem
Wounds:
The Role of Oxygen. New York, NY:
Elsevier Science Publishing
Co Inc; 1988;65-124.
[55.]
Obwegesser
HB, Sailer HF. Experience with intra-oral
resection
and immediate
reconstruction
in cases of
radio-osteomyelitis
of
the mandible. J Maxillofac
Surg.
1978;6:257-261.
[56.]
Marx
RE. A new concept
in
the treatment of
osteoradionecrosis. J Oral
Maxillofac
Surg. 1983;41:351-357.
[57.] Farmer JC Jr,
Sheldon
DL, Angelillo JD, Bennett PD, Hudson
WR. Treatment of
radiation-induced
tissue injury by hyperbaric
oxygen. Ann Otol Rhinol
Laryngol.
1978;87:707-715.
[58.] Davis
JC,
Dunn JM, Gates GA, Heimbach RD. Hyperbaric
oxygen: a new adjunct
in the management of radiation necrosis. Arch
Otolaryngol Head Neck Surg.
1979;105:58-61.
[59.]
Weiss
JP, Boland FP, Mori H, et al.
Treatment of
radiation-induced
cystitis
with hyperbaric oxygen. J Urol.
1985;134:352-354.
[60.] Ferguson BJ, Hudson
WR,
Farmer JC Jr. Hyperbaric oxygen for
laryngeal radionecrosis. Ann
Otol Rhinol Laryngol. 1987;96:1-6.
[61.]
Marx
RE, Johnson RP, Kline
SN.
Prevention of
osteoradionecrosis:
a randomized prospective clinical
trial
of
hyperbaric oxygen versus
penicillin.
J Am Dent Assoc. 1985;111:49-54.
[62.]
Kraut
RA. Prophylactic hyperbaric oxygen
to
avoid
osteoradionecrosis when
extractions follow radiation necrosis.
Arch Otolaryngol Head Neck
Surg.
1985;7:17-20.
[63.] Triplett
RG,
Branham GB, Gillmore JD,
Lorber
M.
Experimental mandibular
osteomyelitis:
therapeutic trials with
hyperbaric oxygen. J Oral
Maxillofac
Surg. 1982;40:640-646.
[64.] Niinikoski J,
Penttinen
R, Kulonen E. Effect of hyperbaric
oxygen on
fracture
healing in the rat: a biochemical study.
Calcif Tissue Res.
1970;4(suppl):115-116.
[65.] Mader JT,
Brown
GL, Guskian JC. A mechanism for the
amelioration by
hyperbaric
oxygen of experimental Staphylococcus
osteomyelitis in rabbits. J
Infect Dis. 1980;142:915-922.
[66.] Davis JC,
Heckman
JD, DeLee JC, Buckwold FJ. Chronic
nonhematogenous
osteomyelitis
treated with adjuvant hyperbaric
oxygen. J Bone Joint Surg Am.
1986;66:1210-1217.
[67.] Strauss MB.
Refractory
osteomyelitis. J Hyperbar Med.
1987;2:146-159.
[68.] Herman
DS.
Hyperbaric oxygen therapy and its role in the
treatment of
chronic
osteomylelitis: a preliminary report
involving refractory
osteomyelitis
in the foot. J Foot Surg.
1985;24:293-300.
[69.] Silver
IA.
Local and systemic factors which affect the
proliferation of fibroblasts.
In: Kulonen E, Pikkarainen J, eds.
The Biology of
Fibroblast.
Orlando, Fla: Academic Press Inc;
1973:507-520.
[70.] Hohn DC, Ponce B,
Burton
RW, Hunt TK. Antimicrobial systems
of the surgical wound, I: a
comparison of oxidative metabolism
and microbicidal
capacity of phagocytes from wounds and from
periferal blood. Am J Surg.
1977;133:597-600.
[71.] Kighton
D,
Silver I, Hunt TK. Regulation of wound healing
angiogenesis: effect
of
oxygen gradients and inspired oxygen
concentration. Surgery.
1981;90:262-270.
[72.] Wyrick WJ, Mader JT,
Butler
E, Hulet WH. Hyperbaric oxygen
in
treatment
of pyoderma
gangrenosum.
Arch Dermatol.
1978;114:1232-1233.
[73.] Bass BH. The
treatment
of varicose leg ulcers by hyperbaric
oxygen. Postgrad Med.
1970;46:407-408.
[74.] Davis
JC,
Buckley CJ, Barr PO. Compromised soft tissue
wounds: correction of wound
hypoxia. In: Davis JC, Hunt TK, eds.
Problem Wounds: The
Role
of Oxygen. New York, NY: Elsevier
Science Publishing Co Inc;
1988:143-152.
[75.] Korn HN,
Wheeler
ES, Miller T. Effect of hyperbaric oxygen
on second-degree burn wound
healing. Arch Surg. 1977;112:732-737.
[76.] Cianci
P,
Lueders H, Lee H, et al. Adjunctive hyperbaric
oxygen reduces the need
for
surgery in 40-80% burns. J Hyperbar
Med. 1988;3:97-101.
[77.] Wiseman DH, Grossman AR. Hyperbaric oxygen in the treatment of burns. Crit Care Clin. 1985;1:129-145.
[78.] Niu AKC, Yang C, Lee HC, Chen SH, Chang LP. Burns treated with adjunctive hyperbaric oxygen therapy: a comparative study in humans. J Hyperbar Med. 1987;2:75-85.
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