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.)
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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) 684-8111,
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.
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