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Source: UHMS http://uhms.org/Indications/LayIndic.htm
  
AIR OR GAS EMBOLISM (BENDS)
Air
or gas embolism occurs when gas bubbles enter arteries, veins and/or capillaries.
This results in reduced blood flow and poor oxygen delivery to the areas
supplied by the affected circulation. If not fatal, gas embolism can result
in severe, long-standing and irreversible physical and emotional disabilities.
There can be weakness or paralysis in the limbs; vision can be impaired
or absent; brain, heart, lung and other organ damage may occur. Limited
use of remaining functions can be sufficiently severe that total disability
results. Those who do not die may be limited to walking with canes, crutches
or walkers. Those more severely disabled may be wheelchair confined or bedridden.
These outcomes may be permanent and may severely impact quality of life.
Maximal medical treatment of the condition is necessary to ensure the best
possible degree of recovery from this potentially disastrous problem. Hyperbaric
oxygen has been shown to reduce the size of bubbles obstructing circulation.
The increased pressure in the hyperbaric chamber reduces bubble size and
drives the remaining gas into physical solution, while the high oxygen pressure
washes out inert gas from the bubble. When bubbles are smaller or resolved,
blood flow resumes. Poorly oxygenated tissues then receive higher levels
of oxygen delivery. Another problem in gas embolism is that vessels obstructed
by bubbles may leak fluid into surrounding tissues, resulting in swelling.
Such swelling can further reduce tissue blood flow. When flow is restored,
the local swelling will subside with resultant improvement in circulation
and oxygen supply. Finally, the high levels of oxygen provided in the hyperbaric
chamber have the potential to immediately restore cellular oxygen levels
while blood flow impairment and tissue swelling are being corrected. Hyperbaric
oxygen treatment is the primary treatment for gas embolism and a major review
of reported cases clearly indicates superior outcomes with its use compared
to non-recompression treatment.
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Source: UHMS
http://uhms.org/Indications/LayIndic.htm
  
CARBON MONOXIDE
Carbon
monoxide (CO) is a colorless, odorless gas produced as a byproduct of combustion.
Poisoning occurs by inhalation, either accidentally or intentionally (suicide
attempt). CO poisoning is responsible for an estimated 40,000 emergency
department visits and 1,000 accidental deaths in the United States annually.
Approximately 5-6% of patients evaluated in emergency departments for CO
poisoning are treated with hyperbaric oxygen (HBO2). CO
binds to hemoglobin in red blood cells at the sites usually utilized to
carry oxygen to tissues. Oxygen, and especially hyperbaric oxygen, accelerates
the clearance of CO from the body, thereby restoring oxygen delivery to
sensitive tissues such as brain and heart. This has traditionally considered
to be the mechanism of benefit of HBO2. However, research published in the
past few years has demonstrated a number of other mechanisms of toxicity
from CO. Blood vessel (vascular) injury from CO has been demonstrated to
result from CO-induced production of nitric oxide-derived oxidants and cellular
injury from activated white blood cells (neutrophils). CO also causes direct
central nervous system cellular injury through mechanisms that include disturbance
of energy metabolism and intracellular production of oxygen free radicals.
In animal experiments, hyperbaric oxygen, but not normobaric oxygen (NBO2),
has been demonstrated to block each of these mechanisms of toxicity.
Until ten years ago,
the benefit of hyperbaric oxygen treatment of CO poisoning was demonstrated
by comparing the clinical experience at institutions where HBO2 was used
with that at facilities where it was not available. Since 1989, six randomized
prospective trials have been reported comparing HBO2 with NBO2 treatment
of acute CO poisoning. Of these, three demonstrate improved patient outcomes
with hyperbaric oxygen, two report no difference between the two therapies,
and one remains blinded with regard to the treatment administered. A full
listing of the investigations, as well as a discussion of the study designs
and findings, can be found in the UHMS Hyperbaric Oxygen Therapy Committee
Report (available for purchase through this web site). The
UHMS currently recommends HBO2 treatment of individuals with serious CO
poisoning, as manifest by transient or prolonged unconsciousness, abnormal
neurologic signs, cardiovascular dysfunction, or severe acidosis.
Also see a very nice discussion put forward by Dr. Neil Hampson on the benefits of HBO in CO poisoning in 2001.
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Clostridial
myositis and myonecrosis is an acute, rapidly progressive infection
of the soft tissues commonly known as "gas gangrene." The
infection is caused by one of several bacteria in the group known as
"clostridium." While over 150 species of clostridium have
been identified, only a few commonly cause gas gangrene. The infection
typically spreads from a discrete focus of clostridium within the body.
The original source can actually be within the body, as clostridium
normally live in the gastrointestinal tract. Alternatively, the infection
can originate outside the body, such as when infection results from
contamination of wounds during trauma (e.g. motor vehicle accidents).
Gas gangrene infection
is severe and can advance quickly. Besides replicating and migrating,
the organisms which cause gas gangrene produce poisons known as exotoxins.
Exotoxins are capable of liquefying adjacent tissue and inhibiting local
defense mechanisms which might normally contain a less virulent infection.
As such, the advancing infection of gas gangrene may simply destroy
healthy tissue in its path and spread over the course of hours.
Clostridium bacteria
are "anaerobic," meaning that they prefer low oxygen concentrations
to grow. If clostridium are exposed to high amounts of oxygen, their
replication, migration, and exotoxin production can be inhibited. This
is the rationale for the use of hyperbaric oxygen in the treatment of
gas gangrene. Repeated treatment in the hyperbaric chamber has the
potential to slow the progress of the infection while the two primary
therapies, antibiotics and surgical resection of infected tissue, control
it. The advantages
of hyperbaric oxygen treatment in gas gangrene are twofold. First,
it may be lifesaving because exotoxin production is rapidly halted and
less heroic surgery may be needed in gravely ill patients. Second,
it may be limb and tissue-saving, possibly preventing limb amputation
that might otherwise be necessary.
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Crush
injuries occur when body tissues are severely traumatized such as in
motor vehicle accidents, falls, and gun shot wounds. These injuries
frequently occur in the extremities. When crush injuries are severe,
the rate of complications such as infection, nonhealing of fractures,
and amputations range up to 50%. When
used as an adjunct to orthopedic surgery and antibiotics, hyperbaric
oxygen (HBO2) therapy shows promise as a way to decrease complications
from severe crush injuries. HBO2 increases oxygen delivery to the injured
tissues, reduces swelling and provides an improved environment for healing
and fighting infection. Hyperbaric
oxygen treatments should be started as soon after an injury as possible.
They are usually continued for 5 to 6 days. A number of related conditions,
including compartment syndromes, thermal burns, and threatened replantations
are also benefited by hyperbaric oxygen, as discussed in other sections
in this site.
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When scuba
diving, additional oxygen and nitrogen dissolve in body tissues. The additional
oxygen is consumed by the tissues, but the excess nitrogen must be washed
out by the blood during decompression. During or after ascent this excess
nitrogen gas can form bubbles in the tissues, analogous to the carbon dioxide
bubbles that form when a carbonated beverage container is opened. These
bubbles may then cause symptoms that are referred to as decompression sickness
("DCS" or "the bends"). Trapping of gas within the
lungs during ascent, either because the lung is diseased or because of breath-holding,
can cause bubbles to be forced into the bloodstream ("arterial gas
embolism" or "AGE"), where they can block the flow of blood
or damage the lining of blood vessels supplying critical organs such as
the brain. AGE can also occur in non-divers, due to entry of air into the
body, such as during medical diagnostic or therapeutic procedures. Symptoms
of DCS or AGE can include joint pain, numbness, tingling, skin rash, extreme
fatigue, weakness of arms or legs, dizziness, loss of hearing, and in serious
cases, complete paralysis or unconsciousness. Emergency
treatment of DCS or AGE includes administration of oxygen and measures to
maintain adequate blood pressure, such as lying the patient down and fluid
(either oral or intravenous, depending upon availability and severity of
the illness). Definitive treatment for DCS or AGE is administration of
100% oxygen at increased atmospheric pressure in a hyperbaric chamber (typically
at a pressure 2-3 times greater than normal atmospheric pressure).
While some delay in
transporting a patient to a hyperbaric chamber is usually unavoidable, the
success in relieving symptoms is greater if the treatment is administered
within a few hours after the onset of symptoms. Some improvement might
be expected, particularly in mild cases, even after a day or more of delay.
The vast majority of
cases respond satisfactorily to a single hyperbaric oxygen treatment. Sometimes,
repetitive treatments are recommended until no further improvement can be
observed. A small minority of divers with severe neurological injury may
require 15-20 repetitive treatments. The success of hyperbaric oxygen treatment
for DCS or AGE has borne the test of time, and continues to be the standard
of care for the treatment of these disorders.
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Problem
wounds are those which fail to respond to established medical and surgical
management. Such wounds usually develop in compromised hosts with multiple
local and systemic factors contributing to inhibition of tissue repair.
These include diabetic feet, compromised amputation sites, nonhealing traumatic
wounds, and vascular insufficiency ulcers (ulcers with poor circulation).
All share the common problem of tissue hypoxia (low tissue oxygen level,
usually related to impaired circulation). Diabetic
foot wounds are one of the major complications of diabetes and an excellent
example of the type of complicated wound which can be treated with hyperbaric
oxygen. Fifty percent of all lower extremity amputations in the United States
are due to diabetes, at a cost of more than one billion dollars per year.
It is well known that many diabetics suffer circulatory disorders that create
inadequate levels of oxygen to support wound healing. Hyperbaric
oxygen therapy is a treatment in which patients receive high concentrations
of oxygen under pressure in order to increase the oxygen level in the blood
and tissues. The elevation in tissue oxygen which occurs in the hyperbaric
chamber induces significant changes in the wound repair process that promote
healing. When hyperbaric treatment is used in conjunction with standard
wound care, improved results have been demonstrated in the healing of difficult
or limb threatening wounds as compared to routine wound care alone.
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For purpose
of consideration of the use of hyperbaric oxygen (HBO2) therapy, exceptional
blood-loss anemia is by definition loss of enough red blood cell mass
to compromise sufficient oxygen delivery to tissue in patients who cannot
be transfused for medical or religious reasons. Medical reasons may
include the threat of blood product incompatibility or concern for transmissible
disease. Religious beliefs may prohibit the receipt of transfused blood
products. Red
blood cells (RBCs) contain the respiratory pigment hemoglobin (Hb).
Hemoglobin has the powerful ability to pick up oxygen as RBCs pass through
the blood vessels of the lungs. Hemoglobin then has the equally powerful
ability to offload oxygen in the tissues of the body's organ systems.
If plasma were the only vehicle to deliver dissolved oxygen, each 100
ml of blood flowing to an organ system would carry only 0.3 ml of gaseous
oxygen. The consumption of oxygen by human tissues far exceeds this.
For instance, the kidney extracts approximately 2 ml of oxygen for every
100 ml of blood which circulates through it. From the same 100 ml of
blood, the brain extracts approximately 6.5 ml and the heart 10.5 ml
of oxygen. In
most instances, humans average 15 grams of hemoglobin per 100 cc of
blood. Each gram of hemoglobin transports 1.34 ml of oxygen. This
is in addition to the oxygen carried by plasma. So, 100 ml of blood,
by containing 15 grams of hemoglobin, can carry approximately 20 ml
of gaseous oxygen (1.34 ml X 15 g Hb = 20 ml of oxygen). In
the 1960s, the Dutch thoracic surgeon Boerema demonstrated that one
could exchange transfuse piglets with a simulated plasma mixture of
buffered normal saline (Ringer's Lactate solution), dextrose and dextran.
In this process, blood was removed from the blood vessels and the substitute
liquid (without hemoglobin) replaced. He then pressurized the piglets
in a hyperbaric chamber while the animals breathed 100% oxygen. By
the trick of pressurization, enough oxygen could be dissolved in the
simulated plasma mixture to supply tissue oxygen requirements. This
was enough to adequately sustain the animal, as evidenced by the fact
that the animals survived and could be brought out of the chamber to
be successfully re-exchange transfused with their previously extracted
blood. As
hyperbaric oxygen (or for that matter normobaric oxygen) administered
for long periods can become toxic, intermittent administration of HBO2
is essential. This point has been demonstrated clinically by the American
thoracic surgeon, George Hart. In 1974, he reported a series of 26
severe blood loss patients who were treated with HBO2 as an alternative
to otherwise disallowed red blood cell transfusion. The survival rate
was 70%. Alternative
approaches include use of fluorocarbons or stroma-free hemoglobin.
While potentially promising, these treatment solutions still pose uncertainties
for their potential ability to unfavorably alter the immune system.
While erythropoietin may be used to stimulate the bone marrow to produce
RBCs, HBO2 therapy only complements its use in exceptional blood-loss
anemia.
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Abscess
formation in the brain can be a devastating complication of sinus infections
or bone infections (osteomyelitis) of the skull. Occasionally, abscesses
are seeded from infection occurring in other parts of the body. Brain abscesses
are frequently multiple. One
of the problems in treatment in treatment of brain abscesses relates to
the fact that surgically drainage of their contents is often required for
cure. Unfortunately, normal brain tissue surrounding the abscess may be
unavoidably damaged by such surgery. Fine needle aspiration of the abscesses
is being performed with greater frequency to avoid this problem.
Antibiotics may not
penetrate well into brain abscesses. Furthermore, white blood cells, which
kill infecting bacteria, may not have enough oxygen to effectively eliminate
the infection when functioning deep in the abscess at a distance from their
normal blood supply. It is well known that white blood cells require a minimum
level of oxygen to kill bacteria. Most
intracranical abscesses are caused by with anaerobic bacteria (bacteria
that function optimally in low oxygen concentrations). Hyperbaric oxygen
raises the environmental oxygen level in the region of the abscess, exposing
the bacteria to levels which may inhibit or kill them, as well as providing
sufficient oxygen for white blood cells to exercise their killing power.
The average mortality
from intracranial abscess reported in six large series was 20% when hyperbaric
oxygen (HBO2) was not used. Among the 48 known cases treated with HBO2 to
date, the mortality has been only 370px. Additionally, most of the patients
treated with hyperbaric oxygen have returned to their regular daily activity
after recovery, with less apparent brain damage. Therapy with HBO2 carries
minimal risk, so the risk-benefit ratio is not arguable.
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A number
of types of infections of soft tissue may benefit from adjunct treatment
with hyperbaric oxygen and are included in the category of "necrotizing
soft tissue infections." Names of such clinical syndromes include
crepitant anaerobic cellulitis, progressive bacterial gangrene, necrotizing
fasciitis, and nonclostridial myonecrosis. Gas gangrene (Clostridial
myositis and myonecrosis) is a separate entity and is reviewed elsewhere
in this site. Necrotizing
soft tissue infections may result from either a single strain or a mixed
population of bacteria, typically occurring after trauma, surgery, and/or
around foreign bodies. The individual affected by such infections is
frequently compromised by conditions such as diabetes or vascular disease.
In addition to preexisting
host compromise, necrotizing soft tissue infections themselves may induce
conditions adverse to control of the infection by normal host defense
mechanisms. The infections commonly lower tissue oxygen levels, impairing
the ability of the white blood cells (neutrophils) to fight infection.
Toxins produced by bacteria involved may also inhibit neutrophil activity.
The primary treatments
for necrotizing soft tissue infection are surgical excision of infected
tissue and administration of appropriate antibiotics. In selected cases,
addition of hyperbaric oxygen therapy may be both lifesaving and cost
effective. Hyperbaric oxygen may be beneficial in several ways. Some
of the bacteria involved in necrotizing soft tissue infections are "anaerobic,"
growing most rapidly in a low oxygen environment. In the hyperbaric
chamber, tissue oxygen levels may be raised sufficiently to inhibit
bacterial growth. In addition, hyperbaric oxygen treatment may enhance
the ability of neutrophils to kill bacteria, by a number of different
mechanisms. The
use of hyperbaric oxygen for treatment of necrotizing soft tissue infections
should be individualized. In specific instances where risk of morbidity
and mortality are high, adjunct hyperbaric oxygen therapy should be
considered.
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Osteomyelitis
is an infection of the bone. Refractory osteomyelitis is a bone infection
which has not responded to appropriate treatment. Hyperbaric oxygen increases
the oxygen concentration in infected tissues, including bone. Hyperbaric
oxygen directly kills or inhibits the growth of organisms which prefer low
oxygen concentrations (strict anaerobes). These effects occur through the
oxygen-induced production of toxic radicals or through an indirect effect
medicated through the white blood cells (polymorphonuclear leukocytes).
Conversely, hyperbaric
oxygen has no direct effect on organisms which prefer high oxygen concentrations
(aerobes). In fact, hyperoxic conditions may induce aerobic organisms to
produce increased concentrations enzymes protective against oxygen radicals
(e.g. superoxide dismutase). When hyperbaric oxygen increases the oxygen
tension in infected tissue, however, the oxygen-dependent killing mechanisms
of the polymorphonuclear leukocyte are provided sufficient oxygen to function.
Thus, hyperbaric oxygen treatment provides the necessary substrate (oxygen)
for the killing of aerobic organisms by the polymorphonuclear leukocyte.
Hyperbaric oxygen also
augments the efficacy of bacterial killing by certain antibiotics (aminoglycosides,
vancomycin, quinolones and certain sulfonamides). Hyperbaric oxygen provides
adequate oxygen for fibroblast activity, cells which promote healing in
hypoxic tissues. Finally hyperbaric oxygen prevents polymorphonuclear leukocytes
from adhering to damaged blood vessel linings. This decreases the degree
of inflammation which may accompany the surgical treatment of refractory
osteomyelitis. Hyperbaric
oxygen is used clinically for the treatment of refractory osteomyelitis
as noted above. Hyperbaric oxygen is adjunctive therapy and is used with
appropriate antibiotics, surgery and nutrition. There are open, patients
used as there own controls and randomized clinical studies supporting the
use of HBO for the treatment of refractory osteomyelitis.
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Cancer
treatment has improved significantly over the past decade. Although cure
of the cancer is still the highest priority of treatment, cancer specialists
have come to recognize the ever-increasing importance of quality of life
to the cancer survivor. One-half of the estimated 1.2 million new cases
of invasive cancer will receive radiation therapy as a part of their cancer
treatment. Side effects of this therapy can be very toxic, especially when
combined with chemotherapy. Some people are more sensitive to radiation
damage than others, and there are no reliable tests available as yet to
identify those patients who will experience the worst side effects. Radiation
doses must be adequate to control the cancer; otherwise, there is no purpose
in treating the patient. Most radiation cancer specialists or oncologists
design their treatment protocols to give the best dose to control the tumor
and still have no more than 5% of patients develop severe reactions to treatment.
Radiation side effects
are generally divided into two categories. First, there are those that happen
during or just after the treatment, called acute reactions. Second, there
are those that happen months or even years after the treatment, called chronic
complications. The
acute side effects almost always resolve with time and are treated in such
a way as to address the patient's symptoms. For example, when a patient
has a cancer of the mouth or throat, it becomes very difficult for the patient
to eat during and just after treatment because the lining of the mouth and
throat becomes raw and painful. The cells which make up the linings of the
gastrointestinal tract are sensitive to radiation. Both cancer cells and
the cells that line the gastrointestinal tract have a high rate of growth,
and this rapid growth rate makes them more sensitive to radiation damage.
Fortunately, the normal tissue cells have excellent repair abilities and
within a few weeks after the completion of radiation, this damage is repaired.
In the meantime, the patient is supported with pain medicine and supplemental
nutrition. Unfortunately,
chronic complications often may not get better with time and are likely
to get worse. Almost all chronic radiation complications result from scarring
and narrowing of the blood vessels within the area which has received the
treatment. If this process progresses to the point that the normal tissues
are no longer receiving adequate blood supply, death or necrosis of these
tissues can occur. In the past, a severe level of necrosis would require
surgical removal of the damaged tissue. This would be a devastating blow
for a patient whose cancer has been cured. For example, though it occurs
rarely, a patient who has had cancer of the voice box cured might require
the removal of the voice box due to radiation damage. Chronic radiation
damage is called "osteoradionecrosis" when the bone is damaged
and "soft tissue radionecrosis" if it is muscle, skin or internal
organs which have been damaged by the radiation. Since
the 1970's, surgeons of the head and neck region have come to recognize
the value of hyperbaric oxygen treatments in treating damage of the jaw
bone due to radiation. Hyperbaric oxygen has had some of its most dramatic
successes in treating or preventing damage to the jaw bone as a result of
radiation treatments. It has now also been applied to damage of the brain,
damage of muscle and other soft tissues of the face and throat, damage to
the chest wall, abdomen and pelvis as a result of radiation treatment. Papers
in medical journals also report success in treating damage to the bladder
and intestines due to radiation. The high dose oxygen provided in the hyperbaric
chamber is carried in the patient's circulation to the site of injury to
be available for repair of the damage done by the narrowing and scarring
of the blood vessels. Each treatment typically takes one to two hours, and
usually 30-40 daily treatments are needed for healing radiation damage.
Most insurance companies,
including Medicare, will provide coverage to pay for hyperbaric treatments
for chronic radiation injuries.
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Reconstructing
complex wounds is accomplished by shifting or transferring tissues to the
wound from a different part of the body. A "skin graft" is the
transfer of a portion of the skin (without its blood supply) to a wound.
A "flap" consists of one or more tissue components including skin,
deeper tissues, muscle and bone. Flaps are transferred with either their
own, original blood supply (pedicle flap) or with detached blood vessels
which are attached at the site of the wound (free flap). Skin
grafts survive as oxygen and nutrients diffuse into them from the underlying
wound bed. Long-term survival depends on a new blood supply forming from
the wound to the graft. When the wound bed does not have enough oxygen
supplied to it, the skin graft will at least partially fail. Common causes
for this are previous radiation to the wound area, diabetes mellitus, and
certain infections. In these situations, the availability of oxygen in
the wound bed can be increased with hyperbaric oxygen therapy (HBO2) in
preparation for skin grafting. Additionally, HBO2 can be used after skin
grafting to increase the amount of the graft that will survive in these
compromised settings. Flaps
also require oxygen and nutrients to survive. The outer, visible portion
(usually skin) is furthest from the source of blood supply for the flap.
This is the area most likely to be compromised by inadequate oxygen. Factors
such as age, nutritional status, smoking, and previous radiation result
in an unpredictable pattern of blood flow to the skin. If a flap is found
to have less than adequate oxygen after it has been transferred, HBO2 can
help minimize the amount of tissue which does not survive and also reduce
the need for repeat flap procedures. Partial
or complete failure of the wound reconstruction is very difficult for a
patient and also very expensive. HBO2 can help by assisting in the preparation
and salvage of skin grafts and compromised flaps.
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Thermal
burn injuries, if not fatal, can cause disastrous long-term physical and
emotional disability for the survivor. Especially in closed space fires,
thermal and smoke (products of combustion) damage to the lungs can occur,
requiring in some cases intubation and use of a mechanical ventilator. Burn
injuries characteristically progress to become deeper and more extensive
with time. Peak damage occurs within 3-4 days after the initial burn, and
can be up to 10 times worse than the initial burn injury. In more severe
and/or extensive burns (deep second, third and fourth degree burns), multiple
aggressive surgeries are generally necessary to excise the burned tissue
and later perform skin grafts to cover these areas. Burn injuries can result
in lifelong difficulties, physical limitations, loss of job and employment
opportunities, and significant disfigurement as the body heals from the
injury. In many cases, the burn victim's life is radically changed, literally
overnight. The psychiatric adjustments can be overwhelming. When possible,
these injuries should be treated in centers that specialize in the management
of thermal burns. Adjunctive
hyperbaric oxygen (HBO2) therapy has been shown to limit the progression
of the burn injury, reduce swelling, reduce the need for surgery, diminish
lung damage, shorten the hospitalization, and result in significant overall
cost savings. These benefits are more apparent if therapy is initiated within
6-24 hours of the burn injury. Ideally, the patient should have 3 sessions
in the first 24 hours, twice daily treatments until the process stabilizes,
then continued therapy as indicated for healing enhancement and to support
grafted areas. Indications for HBO2 therapy typically include deep second-degree
and third-degree burns that involve greater than 20% of the total body surface
area, and less extensive burns that involve the face, hands or groin area.
Best results are realized when HBO2 is used as an integral part of an aggressive
multidisciplinary approach to the management of this potentially fatal injury.
HBO2 is a very safe therapy even in seriously injured patients when administered
by those thoroughly trained in HBO2 therapy in the critical care setting
and with appropriate monitoring precautions.
  
Northern Nevada Hyperbaric Center, Your Gateway to Healing.
1698
Meadowood Lane E-mail:
First Floor
Northern Nevada
Reno, Nevada 89502
Hyperbaric Center
(775) 826-2084 (voice)
(775) 826-2087 (fax)
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