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Definition of Hyperbaric Oxygen Therapy
The patient breathes 100% oxygen intermittently
while the pressure of the treatment chamber is increased
to greater than one atmosphere absolute (atm abs). Current
information indicates that pressurization should be at least
1.4 atm abs. This may occur in a single person chamber (monoplace)
or multiplace chamber (may hold 2 or more people). Breathing
100% oxygen at 1 atm abs or exposing isolated parts of the
body to 100% oxygen does not constitute HBO2 therapy.
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Indications for Hyperbaric Oxygen Therapy
Approved Indications:
The following indications are approved uses of hyperbaric
oxygen therapy as defined by the Hyperbaric Oxygen Therapy
Committee. The Committee Report can be purchased directly
through the UHMS
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AIR OR GAS EMBOLISM
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.
References:
Mushkat Y, Luxman D, Nachum Z, David MP, Melamed
Y. Gas embolism complicating obstetric or gynecologic procedures.
Case reports and review of the literature. European Journal
of Obstetrics, Gynecology, & Reproductive Biology 1995;63:97-103.
Boussuges A, Blanc P, Molenat F, Bergmann E, Sainty JM.
Prognosis in iatrogenic gas embolism. Minerva Medica 1995;86:453-457.
Weiss LD, Van Meter KW. The applications of hyperbaric oxygen
therapy in emergency medicine. American Journal of Emergency
Medicine 1992;10:558-568. Kindwall EP. Uses of hyperbaric
oxygen therapy in the 1990s. Cleveland Clinic Journal of
Medicine. 1992;59:517-528. Dutka AJ. Air or gas embolism.
In: Hyperbaric Oxygen Therapy: A Critical Review. Camporesi
EM, Barker AC, eds. Bethesda, MD, Undersea and Hyperbaric
Medical Society, 1991:1-10.
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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.
References:
Thom SR, Fisher D, Xu YA, Garner S, Ischiropoulos
H. Role of nitric oxide-derived oxidants in vascular injury
from carbon monoxide in the rat. Am J Physiol 1999;276:H984-992.
Brown SD, Piantadosi CA. Recovery of energy metabolism in
rat brain after carbon monoxide hypoxia. J Clin Invest 1991;89:666-672.
Hyperbaric Oxygen Therapy Committee. Hyperbaric Oxygen Therapy:
1999 Committee Report. Hampson NB, ed. Kensington, MD: Undersea
and Hyperbaric Medical Society; 1999. Hampson N, Dunford
RG, Kramer CC, Norkool DM. Selection criteria utilized for
hyperbaric oxygen treatment of carbon monoxide poisoning.
J Emerg Med 1995;13:227-231.
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CLOSTRIDIAL MYOSITIS & MYONECROSIS
(GAS GANGRENE)
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 two-fold. First, it may be life-saving
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.
References:
1). Bakker DJ. Clostridial myonecrosis. In
Davis JC, Hunt TK, eds. Problem Wounds: The Role of Oxygen.
New York: Elsevier, 1988:153-172.; 2). Hirn M. Hyperbaric
oxygen in the treatment of gas gangrene and perineal necrotizing
fasciitis: A clinical and experimental study. Eur J Surg
1993;570(Suppl):9-36.; 3). Hyperbaric Oxygen Therapy Committee.
Clostridial myositis and myonecrosis (gas gangrene). In:
Hampson NB, ed. Hyperbaric Oxygen Therapy: 1999 Committee
Report. Kensington, MD: Undersea and Hyperbaric Medical
Society, 1999:13-16.; 4). Stevens DL, Bryant AE, Adams K,
Mader JT. Evaluation of therapy with hyperbaric oxygen for
experimental infection with Clostridium perfringens. Clin
Infect Dis 1993;17:231-237.
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CRUSH INJURY
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, non-healing 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.
References:
Bouachour G, Cronier P, Gouello JP, Toulemonde
JL, Talha A, Alquier P. Hyperbaric oxygen therapy in the
management of crush injuries: A randomized double-blind
placebo-controlled clinical trial. J Trauma 1996;41:333-339.
Gustilo R. Management of Open Fractures and their Complications.
W. B. Saunders, Philadelphia 1982;202-208.
Hyperbaric Oxygen Therapy Committee. Crush injuries, compartment
syndromes, and other acute traumatic ischemias. In: Hyperbaric
Oxygen Therapy: 1999 Committee Report. Hampson NB, ed. Undersea
and Hyperbaric Medical Society, Kensington, MD 1999;17-21.
Strauss M. Crush injury, compartment syndrome and other
acute traumatic peripheral ischemias. In: Hyperbaric Medicine
Practice. Kindwall EP and Whelan HT, eds. Best Publishing,
Flagstaff, AZ 1999;753-778.
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DECOMPRESSION SICKNESS or ILLNESS and
ARTERIAL GAS EMBOLISM
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.
References:
1. Francis TJR, Gorman DF. Pathogenesis of
the decompression disorders. In: Bennett PB, Elliott DH,
eds. The Physiology and Medicine of Diving. Philadelphia:
W.B. Saunders, 1993:454-480.; 2). Elliott DH, Moon RE. Manifestations
of the decompression disorders. In: Bennett PB, Elliott
DH, eds. The Physiology and Medicine of Diving. Philadelphia,
PA: WB Saunders, 1993:481-505.; 3). Moon RE, Sheffield PJ.
Guidelines for treatment of decompression illness. Aviat
Space Environ Med 1997;68:234-243.; 40. Navy Department.
US Navy Diving Manual. Vol 1 Revision 3: Air Diving. NAVSEA
0994-LP-001-9110. Flagstaff, AZ: Best, 1993.; 5). Ball R.
Effect of severity, time to recompression with oxygen, and
retreatment on outcome in forty-nine cases of spinal cord
decompression sickness. Undersea Hyperbaric Med 1993;20:133-145.;
6). Kizer KW. Delayed treatment of dysbarism: a retrospective
review of 50 cases. JAMA 1982;247:2555-8.; 7). Moon RE,
Gorman D: Treatment of the Decompression Disorders. In:
The Physiology and Medicine of Diving. Edited by Bennett
PB, Elliott DH. Philadelphia, PA, Saunders, 1993, pp 506-541.
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ENHANCEMENT OF HEALING IN SELECTED PROBLEM
WOUNDS
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.
References:
Cianci P. Adjunctive hyperbaric oxygen in the
treatment of problem wounds: An economic analysis. In: Kindwall
E, ed. Proceedings of the Eighth International Congress
on Hyperbaric Medicine. San Pedro, CA: Best Publishing.
1984:213-216. Cianci P, Petrone G, Drager S, Lueders H,
Lee H, Shapiro R. Salvage of the problem wound and potential
amputation with wound care and adjunctive hyperbaric oxygen
therapy: An economic analysis. J Hyperbaric Med 1988;3:127-141.
Hunt TK. The physiology of wound healing. Ann Emerg Med
1988;17:1265-1273. Stone JA, Cianci P. The adjunctive role
of hyperbaric oxygen therapy in the treatment of lower extremity
wounds in patients with diabetes. Diabetes Spectrum 1997;10:118-123.
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EXCEPTIONAL BLOOD LOSS – ANEMIA
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 off-load 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.
References:
Adir Y, Bitterman N, Katz E, Melamed Y, Bitterman
H. Salutary consequences of oxygen therapy on the long-term
outcome of hemorrhagic shock in awake, unrestrained rats.
Undersea Hyperbaric Med 1993;22(1):23-30. Boerema I, Meijne
NG, Brummelkamp WH, Bouma S, Mensch MH, Kamermans F, Hanf
S, Van Aalderen A. Life without blood. J Cardiovasc Surg
1960;182:133-146. Castro O, Nesbit AE, Lyles D. Effect of
a perfluorocarbon emulsion (Fluosol-DA) on reticuloendothelial
system clearance function. Am J Hematol 1984;16:15-21.
Advanced Trauma Life Support for Doctors, Instruction Manuel,
Chapter 3, Shock, American College of Surgeons, Chicago
IL, 1997, pp 97-146. Hart G. HBO and exceptional blood loss
anemia. In: Hyperbaric Medicine Practice, Kindwall EP, Whalen
HT, eds. Best Publishing Co, Flagstaff AZ, 1999; 741-751.
Hart GB, Lennon PA, Strauss MB. Hyperbaric oxygen in exceptional
acute blood-loss anemia. J Hyperbaric Med 1987;2:205-210.
Hart GB. Exceptional blood loss anemia. Treatment with hyperbaric
oxygen. JAMA 1974;228:1028-1029.
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INTRACRANIAL ABSCESS
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 2%. 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.
References:
Lampl L, Frey G, Bock KH. Hyperbaric oxygen
in intracranial abscesses - update of a series of 13 patients
(abstract). Undersea Biomed Res 1992:19(Suppl):83. Mathieu
D, Wattel F, Neviere R, Bocquillon N. Intracranial infections
and hyperbaric oxygen therapy: A five year experience (abstract).
Undersea Hyperbaric Med 1999;26(Suppl):67. Sutter B, Legat
JA, Smolle-Juttner FM. Brain abscess before and after HBO.
12th Proc Sc Soc Physiol, Styria (Austria) 1996.
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NECROTIZING SOFT TISSUE INFECTIONS
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 pre-existing 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.
References:
Mader JT, Adams KR, Sutton TE. Infectious diseases:
Pathophysiology and mechanisms of hyperbaric oxygen. J Hyperbaric
Med 1987;2:133-140. Knighton DR, Fiegel VD, Halverson T,
Schneider S, Brown T, Wells CL. Oxygen as an antibiotic:
The effect of inspired oxygen on bacterial clearance. Arch
Surg 1990;125:97-100. Brogan TV, Nizet V, Waldhausen JHT,
Rubens CE, Clarke WR. Group A Streptococcal necrotizing
fasciitis complicating primary varicella: A series of fourteen
patients. Pediatr Infect Dis Jour 1995;14:588-594. Riseman
JA, Zamboni WA, Curtis A, Graham DR, Konrad HR, Ross DS.
Hyperbaric oxygen therapy for necrotizing fasciitis reduces
mortality and the need for debridements. Surgery 1990;108-847-850.
Hollabaugh RS, Dmochowski RR, Hickerson WL Cox CE. Fournier’s
Gangrene: Therapeutic impact of hyperbaric oxygen. Plast
Reconstruct Surg 1998;101:94-100.
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OSTEOMYELITIS (REFRACTORY)
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.
References:
Mader JT, Guckian JC, Glass DL, Reinarz JA.
Therapy with hyperbaric oxygen for experimental osteomyelitis
due to Staphylococcus aureus in rabbits. J Infect Dis 1978;138:312-318.
Mader JT, Brown GL, Guckian JC, Wells CH, Reinarz JA. A
mechanism for the amelioration by hyperbaric oxygen of experimental
staphylococcal osteomyelitis in rabbits. J Infect Dis 1980;142:915-922.
Davis JC, Heckman JD, DeLee JC, Buckwold FJ. Chronic non-hematogenous
osteomyelitis treated with adjuvant hyperbaric oxygen. J
Bone Joint Surg 1986;68A:1210-1217. Mader JT, Shirtliff
ME, Calhoun JH. The Use of Hyperbaric Oxygen in the Treatment
of Osteomyelitis. In: Hyperbaric Medicine Practice. Best
Publishing Co. Flagstaff, Arizona. 1999;603-616. Mader JT,
Calhoun JH. Osteomyelitis. In: Principles and Practice of
Infectious Diseases. GL Mandell, RG Douglas, JE Bennett
Jr. (Eds). Churchill Livingstone, New York, NY: 5th Edition.
1999;1039-1051.
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COMPLICATIONS OF RADIATION THERAPY
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.
References:
Marx RE, Johnson RP, Kline SN. Prevention of
osteoradionecrosis: A randomized prospective clinical trial
of hyperbaric oxygen versus penicillin. J Am Dent Assoc
1985;11:49-54. Hart GB, Mainous EG. The treatment of radiation
necrosis with hyperbaric oxygen. Cancer 1976;37:2580-2585.
Feldmeier JJ, Heimbach RD, Davolt DA, Brakora MJ. Hyperbaric
oxygen as an adjunctive treatment for severe laryngeal necrosis:
A report of nine consecutive cases. Undersea Hyper Med 1993;20:329-335.
Marx RE. Radiation injury to tissue. In: Kindwall EP, ed.
Hyperbaric Medicine Practice. Flagstaff, Best Publishing,
1995, pp 464-503. Feldmeier JJ, Newman R, Davolt DA, Heimbach
RD, Newman NK, Hernandez LC. Prophylactic hyperbaric oxygen
for patients undergoing salvage for recurrent head and neck
cancers following full course irradiation (abstract). Undersea
Hyper Med 1998;25(Suppl):10. Feldmeier JJ, Heimbach RD,
Davolt DA, Court WS, Stegmann BJ, Sheffield PJ. Hyperbaric
oxygen as an adjunctive treatment for delayed radiation
injury of the chest wall: A retrospective review of twenty-three
cases. Undersea Hyper Med 1995;22(4):383-393. Bevers RF,
Bakker DJ, Kurth KH. Hyperbaric oxygen treatment for haemorrhagic
radiation cystitis. Lancet 1995;346:803-805. Woo TCS, Joseph
D, Oxer H. Hyperbaric oxygen treatment for radiation proctitis.
Int J Radiat Oncol Biol Phys 1997;38(3):619-622. Warren
DC, Feehan P, Slade JB, Cianci PE. Chronic radiation proctitis
treated with hyperbaric oxygen. Undersea Hyper Med 1997;24(3):181-184.
Feldmeier JJ, Heimbach RD, Davolt DA, Court WS, Stegmann
BJ, Sheffield PJ. Hyperbaric oxygen as an adjunctive treatment
for delayed radiation injuries of the abdomen and pelvis.
Undersea Hyper Med 1997;23(4):205-213. Feldmeier JJ, Heimbach
RD, Davolt DA, Stegmann BJ, Sheffield PJ. Hyperbaric oxygen
as an adjunct in the treatment of delayed radiation injuries
of the extremities (abstract). Undersea Hyper Med 1998;25(Suppl);9.
Fontanesi J, Golden EB, Cianci PC, Heideman RL. Treatment
of radiation-induced optic neuropathy in the pediatric population.
Journal of Hyperbaric Medicine 1991;6(4):245-248. Chuba
PJ, Aronin P, Bhambhani K, Eichenhorn M, Zamarano L, Cianci
P, Muhlbauer M, Porter AT, Fontanesi J. Hyperbaric oxygen
therapy for radiation-induced brain injury in children.
Cancer 1997;80:2005-2012. Pomeroy BD, Keim LW, Taylor RJ.
Preoperative hyperbaric oxygen therapy for radiation induced
injuries. J Urol 1998;159:1630-1632.
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SKIN GRAFTS AND FLAPS (COMPROMISED)
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.
References :
1. McFarlane RM, Wermuth RE. The use of hyperbaric
oxygen to prevent necrosis in experimental pedicle flaps
and composite skin grafts. Plast Reconstr Surg 1966;37:422-430.;
2). Greenwood TW, Gilchrist AG. The effect of HBO on wound
healing following ionizing radiation. In: Trapp WC, ed.
Proceedings of the Fifth International Congress on Hyperbaric
Medicine, Vol 1. Barnaby, Canada: Simon Frasier University,
1973:253-263.; 3). Tan CM, Im MJ, Myers RA, Hoopes JE. Effect
of hyperbaric oxygen and hyperbaric air on survival of island
skin flaps. Plast Reconstr Surg 1974;73:27-30.; 4). Zamboni
WA. Applications of hyperbaric oxygen therapy in plastic
surgery. In: Oriani G, Marroni A, Wattel F, eds. Handbook
on Hyperbaric Oxygen Therapy. New York: Springer-Verlag,
1996.
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THERMAL BURNS
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.
References:
Cianci P, Lueders HW, Lee H, Shapiro RL, Sexton
J, Williams C, Sato R. Adjunctive hyperbaric oxygen therapy
reduces length of hospitalization in thermal burns. J Burn
Care Rehabil 1989;10:432-435. Cianci P, Sato R. Adjunctive
hyperbaric oxygen therapy in treatment of thermal burns:
a review. Burns 1994;20(1):5-14. Cianci P, Lueders H, Lee
H, Shapiro R, Sexton J, Williams C, Green B. Adjunctive
hyperbaric oxygen reduces the need for surgery in 40-80%
burns. J Hyper Med 1988;3:97. Cianci P, Williams C, Lueders
H, Lee H, Shapiro R, Sexton J, Sato R. Adjunctive hyperbaric
oxygen in the treatment of thermal burns - an economic analysis.
J Burn Care Rehabil 1990;11:140-143.
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SELECTED SUPPORTIVE REFERENCES
ACUTE
CARBON MONOXIDE INTOXICATION
Bartlett, R: Carbon
monoxide poisoning. Clinical management
of poisoning and drug overdose. WB Saunders, Lester M Haddad,
James F Winchester editors; 3rd edition; 1997. General
review article, emphasizing both the modern appreciation
of the complex pathophysiology involved, and the multifactorial
benefits of HBO therapy.
Thom, SR: Carbon
monoxide-mediated brain lipid peroxidation in the rat.
J. Appl. Physiol. 1990;68(3): 997-1003.
A publication that advanced the pathophysiology
of CO poisoning from the simple concept of inhibition of
hemoglobin function. This data indicates that critical cellular
toxicity occurs.
Thom, SR: Antagonism
of carbon monoxide-mediated brain lipid peroxidation by
hyperbaric oxygen. Toxicol. Appl.
Pharmacol. 1990; 105: 340-344. In
reference to the above elucidation of a cellular poisoning,
this companion study demonstrates the ability of HBO therapy
to inhibit the toxic process.
Thom, SR:
Leukocytes in carbon monoxide-mediated brain oxidative injury.
Toxicol. Appl. Pharmacol. 1993;
123: 243-247. Recent evidence
of complex tissue injury, here involving a leukocyte –mediated
brain injury as a result of acute CO poisoning.
Thom, SR: Functional
inhibition of leukocyte B2 integrins by hyperbaric oxygen
in carbon- monoxide-mediated brain injury in rats.
Toxicol. Appl. Pharmacol. 1993; 123:
248-256. A companion article
to that pathophysiology noted in the previous article. This
research demonstrates the functional inhibition of leukocytes
by HBO therapy, thereby antagonizing CO medicated oxidative
brain injury. Clearly, CO poisoning involves multiple and
complex pathologies. Hyperbaric oxygen has been consistently
demonstrated as antagonistic to these processes: something
no other intervention, including oxygen delivered without
a hyperbaric chamber, has been demonstrated.
Myers RAM, Snyder SK, Emhoff TA:
Subacute sequelae of carbon monoxide
poisoning. Ann Emerg Med. December
1985; 14: 1163-1167. A large
case series that reports the ability of HBO therapy to minimize/eliminate
post exposure relapse, which occurred in 12% of CO poisoned
patients not treated hyperbarically. The reader is asked
to consider the morbidity and cost (work-related absence,
etc.) associated with such sequelae.
Norkool DM, Kirkpatrick JN:
Treatment of acute carbon monoxide poisoning
with hyperbaric oxygen: A review of 115 cases. Ann
Emerg Med. December 1985; 14: 1168-1171. Further
evidence of the significant (43%) relapse/ late complications
that characterize CO poisoned patients who do not receive
hyperbaric oxygenation.
Van Hoesen KB, Camporesi EM, Moon
RE, Hage ML, Piantadosi CA: Should
hyperbaric oxygen be used to treat the pregnant patient
for acute carbon monoxide poisoning? A case report and literature
review. JAMA 1989; 261: 1039-1043.
A report of the heightened risk/morbidity/mortality
to the fetus in maternal CO poisoning. The authors provide
a recommended management protocol that centers around HBO
therapy.
McNulty JA, Maher BA, Chu M, ET AL.:
Relationship of short-term verbal memory
to the need for hyperbaric oxygen treatment after carbon
monoxide poisoning. Neuropsychiatry,
Neuropsychology and Behavioral Neurology 1997;10: 174-179.
A case controlled study demonstrating
the benefit of HBO therapy in improving short-term memory
following CO exposure.
Thom SR, Taber RL, Mendiguren II,
Clark JM, Hardy KR, Fisher AB: Delayed
neuropsychologic sequelae after carbon monoxide poisoning:
prevention by treatment with hyperbaric oxygen. Annuals
of Emergency Medicine. April 1995; 25:4: 474-480.
Prospective randomized clinical trial
that confirms the findings of above noted and non-controlled
reports: namely: HBO therapy "decreased the incidence
of delayed neurological sequelae after CO poisoning."
Ducasse JL, Celsis P, Marc-Vergnes
JP: Non-comatose patients with
acute carbon monoxide poisoning: hyperbaric or normobaric
oxygenation? Undersea Hyperbaric
Med 1995; 22(1): 9-15. Prospective
and randomized blinded clinical trial. The authors conclude
that HBO therapy "reduces the time of initial recovery
and the number of delayed functional abnormalities…"
Jiang J, Tyssebotn I: Normobaric
and hyperbaric oxygen treatment of acute carbon monoxide
poisoning in rats. Undersea Hyperbaric
Med 1997; 24(2): 107-116. A
comparative trial of various groups; involving no treatment,
pressurized air treatment and pressurized oxygen treatment,
in a severe CO and cerebral ischemic model. "Compared
to normoxic treatments, the HBO… significantly reduced
the mortality and neurologic morbidity." HBO was also
significantly better than ‘normal oxygen’ in
increasing survival rate…"
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DECOMPRESSION ILLNESS (or SICKNESS)
Note: In the context of
the Medicare 35-10 document, this "Covered Condition"
refers to Decompression Sickness. Modern (post-1995) terminology
defines Decompression Illness as the syndrome of gas-induced
disease that encompasses both Gas Embolism and Decompression
Sickness. This evolution is, in part, the result of the
frequent difficulty in distinguishing these conditions when
they involve a barotraumatic etiology.
Anon: U.S.
Navy Diving Manual, Volume 1 (Air Diving) 1993; Revision
3:8-22--8-28. Best Publishing Company, Flagstaff, Arizona.
The authoritative text of the
United States military government. It states, among other
things, that "Any decompression sickness that occurs
must be treated with recompression (hyperbaric oxygen therapy)".
Anon: NOAA
Diving Manual, Diving for Science and Technology
1991;20-8--20-9. The authoritative
text of the United States civilian government. It states,
among other things, "The only adequate treatment for
… gas embolism in divers is recompression in a recompression
(hyperbaric) chamber".
Rudge FW, Shafer, MR: The
effect of delay on treatment outcome in altitude-induced
decompression sickness. Aviat. Space Environ. Med.
1991;62:687-690. A military government
review of 232 cases of decompression sickness. The success
of treatment was inversely related to delay in treatment.
Stated differently, closure or non-availability of local
and regional hyperbaric treatment facilities is likely to
result in career/occupatiol ending sequelae, with the not
insignificant longitudinal health costs associated with
rehabilitation and supportive care.
Melamed Y, Shupak A, Bitterman H:
Medical problems associated with underwater
diving. The New England Journal of Medicine 1992;326(1):30-35.
A comprehensive review article. It
identifies a critical diagnostic issue in that subtle neurological
injury may co-exist with less severe musculoskeletal involvement.
Non-diving/hyperbaric specialists may well miss this point,
resulting in inappropriate treatment, and long term (and
costly)morbidity.
Hallenbeck JM, Bove AA, Elliott DH:
Mechanisms underlying spinal cord damage
in decompression sickness. Neurology 1975;25:308-316.
A fundamental determination
of the evolution of decompression sickness, demonstrating
obstruction and ischemia of the spinal cord venous drainage,
resulting in infarction. No intervention other than hyperbaric
oxygenation has been tried or proposed as therapeutically
appropriate and able to reverse this process. Pharmacologic
adjuncts are actively under investigation. However, the
fundamental issue is reduction/elimination of gaseous emboli.
Hyperbaric pressurization must, therefore, be considered
mandatory.
VanDerAue OE, Duffner GJ, Behnke AR:
The treatment of decompression sickness:
an analysis of one hundred and thirteen cases. The
Journal of Industrial Hygiene and Toxicology 1947;29(6):359-366.
An historically important paper. It
describes, in a large clinical series, the effectiveness
of hyperbaric therapy in the successful resolution of wide-ranging
presentations, involving both the nervous and musculoskeletal
systems.
Millington T: "No
tech" technical diving: the lobster divers of La Mosquitia.
SPUMS Journal 1997;27(3):147-148. An
example of the resulting human toll when decompression sickness
sufferers do not undergo hyperbaric oxygen therapy. "Inundated
with paralyzed divers".
Green JW, Tichenor J, Curley MD:
Treatment of type I decompression sickness
using the U.S. Navy treatment algorithm. Undersea
Biomed Res 1989;16(6):465-470. A 20-year
review of central nervous system decompression sickness.
"Inappropriate practices such as ….Non-treatment
… resulted in a high incidence of deterioration or
relapse".
Rivera JC: Decompression
sickness among divers: an analysis of 935 cases.
Military Medicine 1964:314-334. The
U. S. Navy’s experience, involving almost 1,000 cases.
It, again, demonstrates the efficacy of immediate hyperbaric
treatment.
Moon RE: Treatment
of gas bubble disease. Problems
in Respiratory Care 1991;4(2):232-252.
Comprehensive review article.
Moon RE, Sheffield PJ: Guidelines
for treatment of decompression illness.
Aviation, Space, and Environmental Medicine 1997;68(3):234-243.
Consensus statement/guidelines for
the treatment of decompression sickness, based upon a scientific
workshop involving an internationally-respected faculty.
"Definitive treatment … incorporates compression
and administration of breathing gas with elevated partial
pressures of oxygen". "Rapid administration of
pressure and oxygen is paramount …"
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GAS EMBOLISM
Anon: U.S.
Navy Diving Manual, Volume 1 (Air Diving) 1993, Revision
3:8-18--8-20. Best Publishing Co., Flagstaff, Arizona.
The authoritative text of the United States military government.
It notes, among other things, that "… unless
treated promptly and properly by recompression (hyperbaric
oxygen therapy), arterial gas embolism is likely to result
in death or permanent brain damage."
Anon: NOAA
Diving Manual, Diving for Science and Technology
1991, 20-9--20-13. The authoritative
text of the United States civilian government. It states,
among other things, that "Prompt recompression (hyperbaric
oxygen therapy) is the only treatment for gas embolism."
Waite CL, Mazzone WF, Greenwood, ME,
et al: Cerebral air embolism,
I. Basic studies. Submarine Medical Research Laboratory,
U.S. Naval Submarine Medical Center Report No. 493:1-14.
Historically significant publication
from the U.S. Navy Bureau of Medicine and Surgery. It compares
hyperbaric treatment to no hyperbaric treatment in an open-brain
model of gas embolism. Dogs not treated hyperbarically "all
died or were left with severe residual neurological defects".
All of the hyperbarically-treated animals made a complete
recovery, with one exception. This research paved the way
for the modern hyperbaric treatment protocols for gas embolism.
Moon RE: Gas
embolism. Handbook on Hyperbaric Medicine, Eds. Oriani
G, Marroni A, Wattel F. Springer, Italy 1966:229-248. Comprehensive
review article.
Helps SC, Gorman DF: Air
embolism of the brain in rabbits pretreated with mechlorethamine.
Stroke 1991;22:351-354. The third
in a series of articles published in STROKE by these authors.
They have demonstrated a more complex pathophysiology than
that previously appreciated. Cerebral arterial embolization
results in flow deficit, ischemia, followed by a reperfusion-like
injury component in many cases. Such ischemia-reperfusion
complications require the presence of leukocytes. Hyperbaric
oxygen is necessary to support areas of critical flow impairment.
Hyperbaric oxygen will also serve to antagonize leukocyte-mediate
ishemic-reperfusion injury (see #5, Acute Traumatic Peripheral
Ischemia, Article #9, Zamboni, et al).
Reasoner DK, Dexter F, Hindman BJ,
et al: Somastosensory evoked potentials
correlate with neurological outcome in rabbits undergoing
cerebral air embolism. Stroke 1996;27(10):1859-1864.
Validation of the Helps and Gorman’s
(above) model of using evoked potentials to correlate neurological
outcome in gas embolism.
Kol S, Ammar R, Weisz G, et al:
Hyperbaric oxygenation for arterial air
embolism during cardiopulmonary bypass. Ann Thorac
Surg 1993;55:401-403. Representative
paper addressing one of the many iatrogenic etiologies of
gas embolism. It reports the morbidity and mortality associated
with this complication when HBO therapy is not utilized.
It further described the importance of early hyperbaric
referral and treatment.
Bitterman H, Melamed Y: Delayed
hyperbaric treatment of cerebral air embolism. Isr
J Med Sci 1993;29(1):22-26. A report
of the efficacy of HBO therapy in reversal of latent coma,
hemiplegia, and hemiparesis.
Leitch DR, Greenbaum LJ, Hallenbeck:
Cerebral arterial air embolism:
II. Effect of pressure and time on cortical evoked potential
recovery. Undersea Biomed Res 1984;11(3):237-248.
Compares treatment protocols in a
"severe" model of gas embolism " …
no treatment surpassed oxygen at 2.8 bar" (hyperbaric
oxygen therapy).
Leitch DR, Greenbaum, LJ, Hallenbeck:
Cerebral arterial air embolism:
IV. Failure to recover with treatment, and secondary deterioration.
Undersea Biomed Res 1984;11(3):265-274. Comparison
of treatment protocols in a "severe" model of
gas embolism. Hyperbaric doses of air and oxygen were compared
to normobaric (non-hyperbaric) air. In extrapolating this
model to the clinical arena "…the majority of
patients with severe arterial gas embolism will achieve
maximum benefit from compression to 2.8 bar while breathing
oxygen", i.e.,hyperbaric oxygen therapy.
McDermott JJ, Dutka AJ, Koller WA,
et al: Effects of an increased
P02 during recompression therapy for the treatment of experimental
cerebral arterial gas embolism. Undersea Biomed Res
1992;19(6):403-413.
Highly significant outcome improvement
when two standard hyperbaric treatment protocols were compared
to non-hyperbaric air.
Kearns PJ, Haulk AA, McDonald TW:
Homonymous hemianopia due to cerebral
air embolism from central venous catheters. The Western
Journal of Medicine Case Reports 1984;140(4):615-617. Reports
the sustained neurological compromise (infarcts via C.T.
scan) in patients with gas embolism not treated hyperbarically.
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GAS GANGRENE
Bakker DJ: Clostridial
myonecrosis In Problem Wounds, The Role of Oxygen,
Eds. Davis JC and Hunt TK 1988:153-172, Elsevier Publishing
Co., New York. A comprehensive review
article from the institution that has pioneered the medical
and surgical management of gas gangrene over the past four
decades. This reported case series involving bacterially-proven
clostridium perfringens gas gangrene is the largest in the
world,. The report demonstrates that early application of
HBO therapy:
- is life-saving
- is limb- and tissue-saving
- clarifies the demarcation.
Van Unnik AJM: Inhibition
of toxin production in Clostridium perfringens in vitro
by hyperbaric oxygen. Antonie Van Leeuwenhoek 1965;31:181-186.
An historically important in-vitro
study that demonstrated the critical role that Alfa-toxin
plays in the pathophysiology of Clostridium perfringens
(gas gangrene) infections. Further, HBO therapy inhibited
production of this toxin.
Kaye D: Effect
of hyperbaric oxygen on Clostridia in vitro and in vivo.
Proc Soc Exp Biol Med 1967;124:360-366. A
second early study that confirmed the bactericidal properties
of HBO therapy in gas gangrene. HBO was protective, resulting
in decreased mortality.
Hart GB, Lamb RC, Strauss MB:
Gas gangrene: I. A collective review.
The Journal of Trauma 1983;23(11):991-1000. This
two-part report initially provides a 20-year literature
review of gas gangrene, indicating that "a combined
therapy approach with early recognition, surgical intervention,
appropriate antibiotics, and hyperbaric oxygen (HBO) provides
optimal care". The second part summarizes the outcomes
of a large clinical series, supporting the earlier contention
that the addition of HBO therapy to standard surgical and
antibiotic regimes optimizes survival.
Demello FJ, Haglin JJ, Hitchcock CR:
Comparative study of experimental Clostridium
perfringens infection in dogs treated with antibiotics,
surgery, and hyperbaric oxygen. Surgery 1973;73(6):936-941.
A comparative study of gas gangrene
treated with various combinations of surgery, antibiotics
and hyperbaric oxygen. Maximum effectiveness (95% survival)
was achieved when all three modalities were combined.
Hirn M: Hyperbaric
oxygen in the treatment of gas gangrene and perineal necrotizing
fasciitis. Eur J Surg 1993;(570):1-36. A
monograph; it describes both an experimental model and a
clinical series. The animal model resulted in statistically
significant improvement in survival (13% vs. 38%) when HBO
therapy was combined with surgical debridement. Clinically,
HBO reduced mortality through multifactional mechanisms,
which the author describes in detail.
Hirn M, Niinikoski J, Lehtonen OP:
Effect of hyperbaric oxygen and surgery
on experimental gas gangrene. Eur Surg Res 1992;24:356-362.
An experimental model of Clostridial
gas gangrene that reflects modern day medical and surgical
management practices. The findings are entirely consistent
with historic data, in that the addition of HBO therapy
reduced both morbidity and mortality.
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ACUTE TRAUMATIC PERIPHERAL ISCHEMIA
Note: Within the Medicare
35-10 "Covered Conditions" listing are three conditions
for which the rationale for HBO therapy is essentially identical.
These conditions involve different etiologies but the net
insult will frequently follow the common pathway of :acute
ischemia; tissue hypoxia; threatened tissue viability; necrosis;
reperfusion injury, and threatened limb loss.
These conditions are:
- Acute Traumatic Peripheral Ischemia
- Crush Injuries, and Suturing of Severed Limbs.
- Acute Peripheral Arterial Insufficiency
As a consequence of this common disease pathway, the
supportive literature provided below can serve as representative
of all three conditions.
Bouachour MD, Cronier P, Gouello JP,
ET AL.: Hyperbaric oxygen therapy
in the management of crush injuries: A randomized double-blind
placebo-controlled clinical trial. The Journal of
Trauma: Injury, Infection, and Critical Care 1996; 41(2):
333-339. A placebo-controlled randomized
and blinded clinical trial in acute limb-threatening trauma
to the extremities. Statistically significant improvement
in outcome occurred in the HBO group. HBO therapy improved
wound healing, reduced the number of surgical procedures,
and likewise reduced the number of amputations that became
necessary.
Strauss MB, Hart GB.: Crush
injury and the role of hyperbaric oxygen. Topics
in Emergency Medicine 1984; 6: 9-24. An
early review article of HBO’s therapeutic impact in
crush injury. It predated our knowledge of HBO’s effect
on ischemia-reperfusion injury. Consequently, HBO’s
role is even more comprehensivet than described herein.
Lemperle B: Hyperbaric
oxygen therapy for treatment of crush injury and acute traumatic
peripheral ischemia. Health Technology Assessment
Report 1983, DHHS Publ. No. 84-3372:171-182. A
United States Department Health and Human Services, "Health
Technology Assessment Report."
Nylander G, Otamiri T, Lewis DH, ET
AL.: Lipid peroxidation products
in postischemic skeletal muscle and after treatment with
hyperbaric oxygen. Scandinavian Journal of Plastic
Reconstructive Surgery 1989; 23: 97-103. Early
basic science evidence of a therapeutic effect of HBO therapy
in post-ischemia muscle tissue.
Skyhar MJ, Hargens AR, Strauss MB,
ET AL.: Hyperbaric oxygen reduces
edema and necrosis of skeletal muscle in compartment syndromes
associated with hemorrhagic hypotension. Journal
of Bone and Joint Surgery 1986; 68A: 1218-1224. Further
laboratory evidence of the multi factorial benefits that
HBO therapy imparts in acute ischemia/compartment syndrome.
Nylander G. Lewis D. Nordstrom H,
ET AL.: Reduction of postischemic
edema with hyperbaric oxygen. Plastic and reconstructive
surgery 1985; 76(4): 596-601. The
consistent laboratory finding of improved outcomes following
acute peripheral ischemia and treatment with HBO.
Thom SR, Mendiguren I, Hardy K, ET
AL.: Inhibition of human neutrophil
B2-integrin-dependent adherence by hyperbaric o2.
AM J Physiol 1997; 272 (Cell Physiol. 41): C 770-C777. This
paper is included here to demonstrate the depth at which
researchers have investigated in order to elucidate HBO’s
therapeutic effects in ischemia-reperfusion injury.
Strauss MB, Hargens AR, Gershuni DH,
ET AL.: Reduction of skeletal
muscle necrosis using intermittent hyperbaric oxygen in
a model compartment syndrome. The Journal of Bone
and Joint Surgery 1983; 65-A: 656-662. Further
basic science to support the clinical application of HBO
therapy in acute peripheral ischemias: compelling histological
evidence of benefit.
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. Plastic
and Reconstructive Surgery 1993; 91(6): 1110-1123. Using
modern-day laboratory techniques, this work provides firm
morphologic evidence of the beneficial effect of HBO therapy
on microcirculatory perfusion in ischemia-reperfusion injury.
HBO therapy is observed to protect the microcirculation
from an otherwise post ischemia reperfusion injury.
Nylander G, Nordstrom H, Lewis D,
ET AL. Metabolic effects of hyperbaric
oxygen in postischemic muscle. Plastic and Reconstructive
Surgery 1987; 79(1): 91-97. Sub-cellular
evidence of therapeutic effects associated with the application
of hyperbaric hyperoxia in post-ischemic muscle tissue.
The authors conclude that "Hyperbraic oxygen treatments
in the post-ischemic phase stimulate aerobic metabolism."
Radonic V, Baric D, Giunio L, ET AL.:
War injuries of the femoral artery and
vein: A report on 67 cases. Cardiovascular Surgery
1998; 5 (6): 641-647. A clinical series
of war wounded patients. "Hyperbaric oxygen therapy
should be used in selected cases in order to improve tissue
oxygenation, wound healing, host defense mechanisms, and
therapy."
Shupak A, Gozal D, Melaned AY, ET
AL. Hyperbaric oxygenation in
acute peripheral posttraumatic ischemia. Journal
of Hyperbaric Medicine 1987; 2 (1): 7-14. A
second clinical series of patients suffering acute post-traumatic
limb ischemia. The authors stress the important adjunctive
role of HBO therapy.
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PROGRESSIVE NECROTIZING INFECTIONS
Green RJ, Dafoe
DC, Raffin TA: Necrotizing fasciitis.
Chest 1996;110(1)219-229. A
recent review of necrotizing fasciitis, published in CHEST.
With regard to hyperbaric oxygen, the authors conclude that
where available, "it should be considered as a treatment
adjunct in patients with necrotizing fasciitis."
Knighton DR, Halliday B, Hunt TK:
Oxygen as an antibiotic: the effect of
inspired oxygen on infection. Arch Surg 1984;119:199-204.
This reference is included to emphasize
an important feature of HBO therapy in infectious diseases.
Hyperbaric doses of oxygen take on antibiotic-like properties.
The paper stresses the importance of sufficient local oxygen
tension in order that bacterial killing by leukocytes can
be accomplished.
Knighton DR, Halliday B, Hunt TK:
Oxygen as an antibiotic: a comparison
of the effects of inspired oxygen concentration and antibiotic
administration on in vivo bacterial clearance. Arch
Surg 1986;121:191-195. The same authors
cited in the previous paper demonstrate an additive effect
when elevated oxygen tensions are combined with antibiotics.
Mader JT, Guckian JC, Glass DL, et
al: Therapy with hyperbaric oxygen
for experimental osteomyelitis due to staphylococcus aureus
in rabbits. The Journal of Infectious Diseases 1978;138(3):312-318.
The third of three papers that provide
important mechanistic support for HBO therapy in infected
tissue. In this case, HBO improves leukocyte antimicrobial
function.
Bakker DJ: Pure
and mixed aerobic and anaerobic soft tissue infections.
Hyperbaric Oxygen Review 1985;6(2):65-96. A
review article, with emphasis on the role of hyperbaric
oxygen therapy. The author further presents 50 cases from
his institution.
Hirn M: Hyperbaric
oxygen in the treatment of gas gangrene and perineal necrotizing
fasciitis. Eur J Surg 1993;(570):1-36. A
monograph; it describes an experimental model of both necrotizing
fasciitis and gas gangrene, a clinical series, and a literature
review. HBO therapy decreases mortality, clarifies the demarcation
of necrotic vs. potentially viable tissue (improved limb
salvage), and enhances wound healing.
Riseman JA, Zamboni WA, Curtis A,
et al: Hyperbaric oxygen therapy
for necrotizing fasciitis reduces mortality and the need
for debridements. Surgery 1990;108:847-850. A
clinical study of 29 patients, in which outcome was compared
between a surgery and antibiotics group and a surgery, antibiotics,
and HBO therapy group. The addition of HBO "…
significantly reduced mortality and wound morbidity/number
of treatments".
Gozal D, Ziser A, Shupak A, et al:
Necrotizing fasciitis. Arch Surg
1986;121:233-235. A small clinical
series in which the combined approach of surgery, antibiotics
and HBO therapy resulted in a mortality of 12.5%. This compared
with mortality rates as high as 72.7% noted in the paper’s
review of the disease treated without HBO.
Pizzorno R, Bonini F, Donelli A, et
al: Hyperbaric oxygen therapy
in the treatment of Fournier’s disease in 11 male
patients. The Journal of Urology 1997;158:837-840.
A clinical series of the "Fournier’s
Disease" aspect of necrotizing soft tissue infections.
The authors, while recognizing their small number of patients,
felt that their results "underline the importance of
hyperbaric oxygen therapy …"
Hollabaugh RS, Dmochowski RR, Hickerson
EL, et al: Fournier’s gangrene:
therapeutic impact of hyperbaric oxygen. Plast. Reconstr.
Surg. 1998;101(1):94-100. A very recent
clinical series involving two largely equal groups, with
HBO therapy as the variable. Mortality was 7% in the HBO
group compared to 42% in those not receiving HBO (statistical
significance at the 0.05 level).
McHenry CR, Piotrowski JJ, Petrinic
D, et al: Determinants of mortality
for necrotizing soft-tissue infections. Ann. Surg.
1995;221(5):558-565. Contrast the
previous papers with that presented in this oft-quoted paper
that reported improved mortality (29%!) vs. previous literature.
The authors discounted HBO therapy’s efficacy and
suggested that its use will delay debridement. Typically,
HBO therapy does not precede surgery, therefore, such delays
do not occur.
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PREPARATION AND PRESERVATION OF
COMPROMISED SKIN GRAFTS
Note: Problem wound healing
frequently occurs in patients who are systemically or locally
host compromised. Regardless of underlying etiology, tissue
hypoxia is the most common denominator. When operative repair
is necessary, surgeons turn to the Reconstructive Ladder,
a series of graft and flap options of increasing complexity.
For skin grafts to be considered, the recipient bed
must be of the health and quality to accept and nourish
a graft. This is critical, as such grafts are immediately
rendered ischemic/hypoxic upon harvest.
Availability of oxygen is critical to the success of
any skin grafting procedure, and subsequent graft durability.
The following papers chronicle the role of oxygen in the
healing process, and conclude with the application of HBO
therapy in wound healing and limb salvage. Such application
is designed to either:
- prepare the recipient bed for definitive coverage
(grafts or flaps)
- it is recognized that, in some cases, the therapeutic
effect of HBO will be such that skin grafting may be unnecessary
- support skin graft or skin flap procedures, in the
immediate post-operative setting.
Sheffield PJ: Tissue
oxygen measurements with respect to soft-tissue wound healing
with normobaric and hyperbaric oxygen. HBO Review
1985;6(1):18-43. Evidence that hyperbaric
doses of oxygen increase tissue oxygen levels in otherwise
hypoxic and ischemic wounds. This work represents a fundamental
rationale for the application of HBO therapy in the setting
of non-healing lesions, where an underlying hypoxia is demonstrated.
Padberg FT, Back TL, Thompson PN,
et al: Transcutaneous oxygen (TcP02)
estimates probability of healing in the ischemic extremity.
J Surg Res 1996;60(2):365-369. A more
recent evaluation of the relationship between availability
of oxygen and probability of healing in the ischemic extremity.
Transcutaneous oximetry "alone" is sufficient
for objective risk stratification of arterial ischemia in
the lower extremity.
Bunt TJ, Holloway GA: TcP02
as an accurate predictor of therapy in limb salvage.
Ann Vasc Surg 1996;10(3):224-227. Further
evidence of both the role of oxygen in limb salvage, and
the ability of transcutaneous oximetry to identify tissue
beds at risk.
LaVan FB, Hunt TK: Oxygen
and wound healing. Clinics in Plast Surg 1990;17(3):463-472.
This paper summarizes the extensive
amount of basic research (much of which came from these
authors’ laboratory at the University of California,
San Francisco). The authors emphasize the role of HBO therapy
as a "strong stimulus" for angiogenesis. They
further note that HBO is not effective "if blood supply
is insufficient". Hence, the important role of transcutaneous
oxygen in the case management of hyperbarically-referred
patients under the Preparation or Preservation of Compromised
Graft protocol.
Clarke D: An
evidence-based approach to hyperbaric wound healing.
Blood Gas News 1998;7(2):14-20. One
example of an algorithmic approach to hyperbaric wound healing.
The goal is to identify those who possess the physiologic
capability to respond locally (the wound) to centrally-delivered
(HBO) hyperoxia. In those patients, determination of therapeutic
endpoint (when a critical mass of angiogenesis is presumed
to be present) ensures a cost-effective application of this
therapeutic resource
Tompach PC, Lew D, Stoll JL:
Cell response to hyperbaric oxygen treatment.
Int J Oral Maxillofac Surg 1997;26:82-86. More
advanced thinking, and confirmatory study, regarding the
effect of HBO on wound healing. Here, in an in-vitro cell
model, HBO positively influences healing responses at the
cellular level.
Hehenberger K, Brismar K, Lind F,
et al: Dose-dependent hyperbaric
oxygen stimulation of human fibroblast proliferation.
Wound Rep Reg 1997;5(2):147-150. Further
cellular research that demonstrates the dose dependent nature
of oxygen on an important component of the wound healing
module.
Siddiqui A, Davidson JD, Mustoe TA:
Ischemic tissue oxygen capacitance after
hyperbaric oxygen therapy: A new physiologic concept.
Plast Reconstr Surg 1997;99(1):148-155. A
new concept is proposed, one that incorporates previous
evidence of HBO’s benefit in ischemic wound healing,
and is supported by the research presented herein. This
work further demonstrates the superiority of hyperbaric
vs. normobaric oxygen.
Gibson JJ, Hunt TK: Hyperbaric
oxygen potentiates wound healing. Diving and Hyperbaric
Medicine Proc. 23rd EUBS Congress, Bled. Slovenia 1997:153-160.
This paper demonstrates a beneficial
effect of HBO therapy, in a dose-dependent manner, on angiogenesis.
This effect is highly significant when compared to "controls";
air breathing at sea level pressure.
Boykin JV: Hyperbaric
oxygen therapy: A physiological approach to selected problem
wound healing. Wounds 1996;8(6):183-198. A
recent summary article of the role of HBO therapy in problem
wound healing. This paper captures much of the historic
and recent science, and molds it into a clinical algorithm
in order to maximize medical and surgical management.
Hammarlund C, Sundberg T: Hyperbaric
oxygen reduced size of chronic leg ulcers: A randomized
double-blind study. Pjlast Reconstr Surg 1994;93(4):829-833.
An exacting clinical study. The wounds
in question had failed to heal over more than one year.
The healing effect of HBO on these ulcers was highly significant
(p<0.001).
Baroni G, Porro T, Faglia E, et al:
Hyperbaric oxygen in diabetic gangrene
treatment. Diabetes Care 1987;10(1):81-86. One
of the "early" case controlled studies, in which
HBO was evaluated in diabetic foot gangrene. It was not
uncommon for these patients to undergo subsequent grafts
or flap repair, in one form or another, when major limb
salvage is averted. HBO therapy markedly reduced the rate
of such amputations.
Oriani G, Michael M. Meazza D, et
al: Diabetic foot and hyperbaric
oxygen therapy: A ten-year experience. J Hyper | 
