hbot

Saeid Kalbasi MD.
Endocrinologist
Loghman Hospital
October 2012

 Hyperbaric oxygen therapy
 Negative Pressure wound therapy
 Growth factors
 Bioengineered skin substitutes

 Definition, History of Hyperbaric Oxygen therapy
 Terminology and Indications and protocols
 Process of Mediating the Healing of wounds
a.) Collagen synthesis
b.) Angiogenesis
 Rationale for the Use of Oxygen in wounds
 Antibacterial actions
 Reperfusion Injury
 Topical oxygenation
 Complications of HBO therapy

Involves the inhalation of oxygen at partial
pressures meeting or exceeding 1.4 ATA.
---(Whelan,H.T. and Kindwall, E.P. 1999).

 At its inception, lacked a scientific basis.
 Precursors of modern hyperbaric oxygen simply
seemed like good ideas.
Henshaw 1662
 Compressed air therapy resurfaced in the 19th
century in the European continent:
a.) Some of the devices could be pressurized to 2 ATA
(the pressure equivalent of a 33-foot column of sea
water)
b.) Capacity up to 10 occupants.

 Fontaine (1879) and Corning (1891).
a.) Fabricated a mobile operating room on wheels,
b.) Pressurized in concert with the administration of
the anesthetic gas nitrous oxide.
 Benefits of the hyperbaric surgical environment
a.) Reduction in the size of hernias
b.) Decreased cyanosis,
 Corning,
a.) The first physician to administer spinal anesthetic
b.) Imported compressed air therapy into the United
States
c.) Pioneered electrical powering of compressors.

Cunningham,
 Promoted hyperbaric therapy based on epidemiological
observations.
Individuals
A.) heart disease
B.) circulatory problems
Observations
1.) Fared less well than similarly stricken patients dwelling near sea
level.
2.) Patitents at altitude fared better when relocated to sea level.
Hypothesis:
 PRESSURE WAS THE KEY
 Elevation of pressure beyond that characteristic of sea level would
confer even greater benefit.

Case Report
 A young colleague bear death from the flu apparently exhibited a
remarkable recovery in conjunction with hyperbaric therapy.
Early chambers
 Created a large chamber measuring 88 feet in length with a 10-foot
diameter in Kansas City.
Treatment Protocols
 No discrimination for clinical indications met by compressed air
therapy.
 Further hypothesized
 Ailments stemmed from infection with anaerobic bacteria.
 Elevated partial pressures of oxygen would hinder anaerobic
bacteria,
Case report 2
 Kidney patient underwent a nearly miraculous recovery while
under the care of Cunningham.

Results
 Techniques of Cunningham were “miracles”,
 The wealthy patient rewarded Cunningham by constructing
the largest hyperbaric chamber ever to have existed.
 The giant sphere, “Steel Ball Hospital”
a.) Located in Cleveland, Ohio,
b.) Measured an impressive 6 stories in height and 64 feet in
diameter.
c.) Interestingly, the enormous chamber,
 Could sustain pressures of 3 ATA (66 fsw),
 Was lavishly appointed with carpeting, cafeterias, and a top-
floor smoking lounge
 Cost 1,000,000 USD

Results
 Unable to gather data sufficient to support his
broad hypothesis concerning:
A.) Anaerobic bacteria in disease :
(e.g., hypertension, uremia, diabetes and cancer).
 The AMA and Cleveland Medical Society in
1930 forcibly closed the hospital,
 condemning it to scrap for use during World
War II.

 Churchill-Davidson and colleagues (1955)
1.) Were the first to employ elevated
concentrations of oxygen,
2.) Became known as hyperbaric oxygen therapy.
3.) Oxygen was used in attempts to potentiate the
therapeutic effect of radiation in cancer
patients.
 Boerema and associates (1956),
a.) Prolonged tolerance to a circulatory arrest
related to cardiac surgery.

Physical properties of gases under pressure,
 At pressure greater than 1 atm.
 Oxygen is essential in a variety of enzymatic,
biochemical, and physiologic interactions
a.) Promote normal cellular respiration and tissue
function.
b.) Collagen deposition and synthesis
c.) Angiogenesis and epithelization also are
oxygen dependent.

The mechanism
1.) Oxygen from air diffuses across the aveoli
 From the high pressure in the alveoli (pO2 100 mmHg)
to lower pressure pulmonary capillaries (pO2 40
mmHg).
 The pulmonary capillaries carry the deoxyhemoglobin
in the blood from the right ventricle to the lungs.
 After oxygenation blood (carrying oxyhemoglobin)
moves into the pulmonary veins for return to the left
side of the heart to be pumped systemically.

Under normal conditions,
> 97.5% of 02 is carried in the bloodstream bound to
hemoglobin.
 The remaining 2.5% is dissolved in plasma.
 Each gram of hemoglobin combined with 1.34 cm3 of
oxygen.
> physiologic maximum.
> normal conditions, Sa02 hb = 97%, SV02 =70%.
The oxygen content can be calculated with the
following equation:
CaO2=(SaO2 x Hb x 1.34) + .003(PaO2)
> Increase Pa02 = increased dissolved 02 in the blood

At a constant temperature, the volume and
the pressure of a gas are inversely
proportional.
In other words…….
A gas will compress proportionately to the
amount of pressure exerted on it.

1.) Decompression sickness,
2.) Carbon monoxide poisoning,
3) Gas embolism,
4.) Gas gangrene with positive culture for a clostridial species,
5.) Acute osteomyelitis refractory to standard medical
management,
6) Chronic non-healing (problem)
a.) Documented failure of an intensive wound management
program (minimum of 6 weeks)
b.) Failure of surgical management or documentation from a
surgeon of poor tissue oxygenation

7.) Refractory bacterial infections,
8.) Acute traumatic ischemia in a salvageable area,
9.) Radiation necrosis (osteoradionecrosis and soft tissue
radiation necrosis)
10.) Acute cerebral edema
11.) Profound anemia with exceptional blood loss:
a.) only when blood transfusion is impossible or must be
delayed,
12.) Refractory mycoses,
13.) Acute cyanide poisoning,

 Medications like doxorubicin (adriamycin), bleomycin, disulfiram, cis-
platinum and mafemide acetate
 Untreated pneumothorax
 Pregnancy
 Implanted pacemakers-electronic
 Smoking
 No air plane travel 24 hours after HBOT treatment.
 Compressive brain or brainstem lesions e.g. unilateral or bilateral sub-
dural hematoma, intracranial hematoma.
 Sickle Cell and Sickle Cell Trait.

 Upper respiratory
infections/chronic
sinusitis
 Seizure disorders
 Emphysema with
CO2 retention
 Acute asthma
 High fevers
 Claustrophobia
 Otosclerosis
 Congenital
spherocytosis
 Viral infections such as
HIV or RSV

MULTIPLACE CHAMBER MONOPLACE CHAMBER

Chronic wounds
 2 ATA for 90min 3-4 x weekly
Necrotizing infections
 2 ATA for 90 min TID
CO Poisoning
 3 ATA for 30 min
 ( ½ life of CO at 3 ATA pressure 23 min)

 The many forms of wounds
 Contused (unbroken skin),
 Incised (cut tissue),
 Lacerated (torn skin),
 Open (free outward opening),
 Penetrating (affects underlying tissue)
 Perforating (penetrating wound into viscous or
body cavity).

 Problem wounds
 Those failing to respond to the conventional
primary and adjunctive management within an
expected period of time.
 Seen in individuals who do not have normal
patterns or rates of tissue repair.
a.) Numerous operations
b.) Prolonged hospitalizations.
c.) Most common in the lower extremities.

Chief pathological features of problem wounds
 Chronic hypoperfusion and contamination.
 Successful management = Identify etiology and potentially
complicating factors
a.) Advanced age,
b.) Nutritional deficits,
c.) Diabetes mellitus,
d.) Use of tobacco,
e.) Radiation damage,
f.) Hypoxia,
g.) Immunosuppression,
h.) Foreign bodies,
i.) Renal failure,
j.) cCancer

 The injured blood vessels allows the wound space to be filled with plasma and red
blood cells.
 The injured endothelium releases Factor III (thromboplastin), which accelerates the
clotting cascade.
 Clotting factors throughout the plasma are activated, forming thrombin and fibrin.
 The complement system activates and produces various chemoattractive
complement protein fragments.
 Platelets, activated by exposed collagen and activated thrombin, release a number
of factors and cytokines.
 To limit bleeding, traumatized vessels will constrict in response to inputs
a.) ANS
b.) PG’s released by the platelets.
 The healthy vasculature proximal to the injury will dilate and leak plasma in
response to various inflammatory mediators such a histamine, kinins, and
serotonin,

Inflamatory process =
 Hypoxic, acidodic and hyperlactate state
 Neutrophils , fibroblasts, endothelial cells
a.) few mitochondria = rely on anaerobic glycolyis for ATP
 Neutrophilic oxidants, will produce lactate
a.) Even if normal levels of 02 are present
b.) Induce an acidodic environment
The importance
 ADPR SYS
a.) Post translational modification of many proteins
b.) Regulates transcription of collagen and VEGR
c.) Lactate in the wound reduce NAD+ to NADH

Importance of Hypoxia
 Increases lactate within the wound environment,
 This allows the synthesis of collage secondary to (redox)
mechanism
 HOWEVER………..
 Studies have proved that fibroblasts NEED 02
a.) Synthesize collagen
b.) Posttranslational modifications necessary for its cross-linking.
Take home message
 Hypoxia acts as the triggering mechanisms for the repair-related
production of collagen,
 Restoration of oxygenation is required to ensure that the collagen-
dependent processes of repair reach their successful conclusion

 Vasculogenesis,
> Primitive vascular network is established embryologically
from endothelial cells precursors called angioblasts.
 Angiogenesis (i.e., neovascularization)
> Proceeds as preexisting vessels send out capillary buds
(sprouts) to create new vessels.
> Results the chronic inflammatory process and fibrosis.
> Redirection of vasculature seen during growth of tumors.

 Clark et al.(1976), injected autologous wound macrophages into rabbit
corneas to stimulate neovascularization and
 Polverini et al.(1977), discovered that activated peritoneal macrophages
induced more vessel growth than non actviated macrophages in the
corneal angiogenesis assay.
 Jensen et al. (1986), later demonstrated that acellular macrophage-
conditioned media alone was sufficient to cause angiogenesis, therefore
underscoring the role of the angiogenic factor.
 Knighton et al. (Knighton, et al. 1983), for example, demonstrated that
media conditioned by macrophages grown at 15 mmHg pO2, supported
angiogenesis; media conditioned by macrophages grown at 38 mmHg or
76 mmHg did not.
IMPORTANCE:
Despite macrophages and vascular growth factors
a.) The most notable stimulator for angiogenesis is in fact hypoxia,
b.) Similar to initiation of the synthesis of collagen in response to injury.

1.) BMJ 1998;317:1140-1143
Clinical review ABC of oxygen Hyperbaric oxygen therapy
2. ) Pediatr Emerg Care. Maintaining a high index of suspicion for carbon
monoxide poisoning is life saving. 2008 Mar;24(3):198.
3.) AANA J. Oxygen: the two-faced elixir of life. 2008 Feb;76(1):61-8.
4.). Singapore Med J. Hyperbaric oxygen therapy in the management of
diabetic lower limb wounds 2008 Feb;49(2):105-9.
5.) Undersea Hyperb Med. Hyperbaric oxygen pre-breathe modifies the
outcome of decompression sickness. 2006 Nov-Dec;33(6):407-17.

 Angiogenesis and collagen synthesis and deposition
share common triggers,
Zabel et al.(1996).
 Cultured macrophages in 0 or 15mM lactate and then
measured NAD+ and poly (ADP-ribose ) synthesis.
 The cells incubated with lactate demonstrated a 40%
lower NAD+ level and therefore a 40% reduction in poly
adenosine diphosphoribose synthetase.
Constant et al. (1996)
 Measured vascular endothelial growth factor in media
grown in normoxia, hypoxia, 15mM of lactate, or
hypoxia and elevated lactate in combination.

OVERALL:
1.) Hypoxia and lactate alone stimulate an
increase in VEGF
2.) Synthesis of collagen and the initiation of
angiogenesis proceed in relation to metabolic
demand, with hypoxia acting as the trigger.
3.) Maturation of collagen and the finalization of
angiogenesis require normal levels of oxygen.

I.E
 Placing an oxygen-breathing individual in a hyperbaric
chamber:
a.) Raises arterial oxygen tensions 10 - 13 times
b.) The surplus oxygen carried by the arterial blood under
hyperbaric conditions will become available to
wounded tissue
c.) Promoting both the maturation/deposition of collagen
and angiogenesis and thus the closure of the wound.
*****Lactate (associated with hypoxia) is the greatest
trigger for stimulating fibroblasts and macrophages
to initiate the manufacture of collagen and induce
angiogenesis

 Oxygen-independent
 Oxygen-dependent

 More important line of defense against infection)
 Seen in all wounds and contributes to tissue debris and
edema.
 Neutrophils and macrophages enter the wound
environment,
a.) Neutrophils = primary defense
b.) Natural (or nonspecific) immunity,
> Neutrophils and macrophages + complement system
> Rapidly and independently of previous exposure to specific
microorganisms.
> The invading bacteria are opsinized by immunoglobins,
> Complement proteins bind to receptors found on
membranes of neutrophils, culminating in pathogenic
recognition by neutrophils and phagocytosis.

 The respiratory burst first involves the
reduction of molecular oxygen (O2) to the
microcidal superoxide anion (O2 -) via the
NADPH oxidase system,
 Superoxide dismutase catalyzes the
interaction of the two superoxide anions to
reform oxygen and hydrogen peroxide
(H2O2), another antibactericidal oxidant.
 Myeloperoxidase, released by the
azurophilic granules of neutrophils,).
 These halide oxygenation products are the
potent oxidants that attack the membrane
proteins of bacteria, (Hunt, T. 1988).
 The production of oxygen radicals and
killing of pathogens via oxidation proceeds
in relation to the availability of oxygen in
the wound environment, (Park, M., 1999).

Oxygen is often ill-equipped to reach the wound
a.) Impaired vascular delivery.
b.) Further limiting the transport of oxygen to problem wounds
may be the necessarily limited oxygen-carrying capacity of
the blood.
Normal circumstances,
a.) The bulk of oxygen is delivered to tissue via hemoglobin with
plasma carrying a significantly smaller load of oxygen (in
solution).
b.) The concentration gradient may be too small to permit
immunologically sufficient quantities of oxygen to diffuse
from capillaries to the wound.

Under hyperbaric conditions,
a.) Situation changes favorably
b.) The breathing of 100% oxygen allows plasma to
transport a greatly elevated load of dissolved
oxygen
c.) Increases the total load of oxygen transported by
the blood

 Increase the load of oxygen carried by the blood,
 Concentration gradient of oxygen between the blood and the
hypoxic problem wound increases,
 Promotes diffusion of the gas into its otherwise oxygen-poor
target.
 Disruption of metabolism and proliferation of anaerobic
bacteria.
 If cells of the immune system are able to access the wound,
A.) Oxygen-dependent attacks of the immune system on both
anaerobic and aerobic bacteria may increase,
B.) Thereby rendering the wound environment more amenable to
healing.

Ischemia,
 Results from the functional constriction or actual
obstruction of the blood vessel).
 High-energy trauma
 Compartment syndrome,
 Amputated body parts
 peripheral vascular disease
RESULT = Some degree of microcirculatory failure and
hence necrosis
When reperfusion follows necrosis,
a.) There is further injury to the microvasculature,
b.) Leads to further cellular death,
c.) Large partially necrotized muscular areas being
particularly vulnerable to the pathological process.

The cytotoxic effects of
reperfusion
 oxygen-derived free radicals,
A.) Highly unstable molecules
possessing an unpaired
electron in the outer shell.
B.) Hazardous to the
intracellular environment,
Sources:
A) Xanthine oxidase (XO),
which is located in the
microvascular endothelial
cells and
B) Neutrophils which destroy
damaged tissue and
invading bacteria

1.) Ischemia= accumulation
hypoxanthine
2.) membrane-spanning pumps
fail,= increase in intracellular
levels of calcium.
3.) Activates proteases, allowing
the conversion of xanthine
dehydrogenase to XO.
4.) When reperfusion occurs, the
enzyme XO converts
hypoxanthine to xanthine and
the superoxide radical.
5.) hydroxy radical will emerge. .
( Aids neutrophils in the
production of the hydroxy
radical)

During reperfusion,
 Increase in neutrophil adherence to the vascular
endothelium,
 Reflects increasing numbers of neutrophils marginating
and extravasating into the surrounding tissues.
Results:
a.) Local vessels will eventually become ill defined.
neutrophils
Releases free radicals= endothelial damage
induce microcirculatory problems through adherence.

Speculations
 One might predict that increased availability of
oxygen would:
a.) Promote free radical-mediated reperfusion injury.
b.) The increased oxygen-carrying capacity of plasma
under hyperbaric conditions,
 Expect severe reperfusion in .
 The production of free radicals would simply
escalate in concert with increased availability of
oxygen.
 The reverse is actually the case.

 The increase in microvascular flow helps increase tissue
survival and therefore decreases necrosis.
 Decrease neutrophil adherence in the venules,
a.)Decreases, problems associated with neutrophilic
adhesions,
> increase free radicals which= tissue damage
The benefits of HBO on the ischemic tissue
 Systemic
 Inhalation of oxygen at a higher atmospheric pressure
 Greater concentration of oxygen to circulate throughout
the entire body
A.) Suppress of systemic neutrophils.
B.) Increase in superoxide dismutase, which is a free
radical scavenger. Zamboni ( 1992),

 Currently available evidence indicates:
That systemically (rather than locally)
augmented levels of oxygen
mitigate the destructive
consequences of free radicals in
ischemic tissue undergoing
reperfusion.

 Increases in oxygen tension in a chronic wound in
may permit and promote a cascade of events
culminating in the full healing of otherwise
nonhealing tissue.
 Means by which oxygen tensions are increased in
such a fashion involves the inspiration of 100%
oxygen under substantially elevated ambient
pressures.
 Henrys Law, allows oxygen to diffuse readily from
capillaries to otherwise inaccessible insufficiently
vascularized tissue, thereby initiating oxygen-
dependent cascades related to healing.

“Men are nothing without Gods”
Homer’s Odyessy

The rational for the topical approach is simple:
 Some investigators believe that topical oxygen
dissolves in sufficient quantity
a.) Exert bactericidal and angiogenic effects,
Marketed aggressively by companies such as
 GWR Medical, Hyperbaric solutions Inc.,
 Sandia-Numotech partnership, which was
established in 1998 to create home-use topical oxygen
applicators.

The device
 The devices employed in the topical application of
oxygen typically consist of a compartment to encase
the affected portion of the body.
 When connected to a regulated flow of oxygen
from commercially available tanks, the
compartment is intended to provide the wound
with a therapeutic oxygen-rich external
environment,
 The compartments (commonly called canopies) that
enclose the wound may be box-like or function as
disposable plastic bags

Acute or chronic wounds such as skin ulceration
a.) Diabetes,
b.) venous stasis,
c.) Post surgical infection,
d.) Decubitus ulcers (pressure ulcers),
e.) Skin grafts,
f.) Frost bites,
g.) Amputations,
h.) Grangrenous lesions,
i.) Burns
Contraindications:
1.) Inadquate perfusion to support healing,
2.) Wounds completely covered with eschar,
3.) Wounds with fistulae or deep sinus tracts where the end cannot be
probed,
4.) Wounds covered with petroleum based dressing,
5.) non-compliant patients.

 Medical history,
 Allergies,
 Current medications,
 Psychological status (to predict compliance),
 Nutritional status,
 Wound description.
***NO ABI’s, NO AGRAM, NO MRA

 Debridement of the wound with removal of thick eschar.
 Culturing of the wound to detect pseudomonas (pseudomonas grows
in an oxygen-enriched environment).
 If pseudomonas is detected, 1% acetic acid is applied with a gauze
dressing, which remains in place during exposure to topical oxygen.
 All creams, ointments, and lotions must be removed as well as all
dressings (except when wounds are positive for pseudomonas) before
oxygen is applied topically.
 8. Treatment will cease if improvement does not occur within 28 d

 Applied for either 90 minutes (twice per day) or during a
single session lasting 180 minutes.
 The lesion should be covered with a moist environmental
dressing following each treatment.
 Before and after each treatment, the topical oxygen canopy
must be cleaned with antiseptic. A culture of the appliance
must be taken periodically to make prevent contamination
of wounds by the apparatus.
 This protocol will not be followed and treatment will not be
administered in the patient has acute thrombophlebitis or if
there is minimal blood supply to the lesion.

 Inability to complete collagen synthesis and
angiogenesis
 Inability to produce a bactericidal effect
 Inability to prevent reperfusion injury

 Henry’s Law is relevant to the reversal of hypoxia associated with the
administration of hyperbaric oxygen.
 Delivery with HBO increase arterial oxygen tensions by 6 volumes
percent,
 Solubility of 02 plasma increases greatly as a function of pressure.
 Importance =
1.) Systemic elevations of oxygen tensions depend on the combination of
substantially elevated pressure (e.g., 2.4 ATA) and pulmonary delivery of
the gas.
2.) A patient is undergoing topical oxygenation of a wound continues to
breathe air at ambient pressure.
 Henry’s Law dictates that,
A.) Even if adequate blood flow and hematocrit are maintained,
plasma at the level of the wound will not suspend significantly more
oxygen.

NO elevated load of oxygen in plasma,
 One can readily predict the failure of
a.) Oxygen-dependent maturation of collagen
b.) Angiogensis
Henry’s Law predicts
a.) Topical oxygenation does not elevate the load of
dissolved oxygen available to problematically
wounded ischemic tissue,
Problem wounds will remain as problems, even in
the face of aggressive topical oxygen therapy.

 Hyperbaric oxygen may exert bactericidal effects
A.) Anaerobic species as demonstrated Hill et al, (1972)
(hyperbaric oxygenation and Clostridium species of bacteria).
B.) Enhance the ability of the immune system to kill even aerobic
bacteria, (Ollodart, 1966).
 Topical Oxygenation
a.) Look at the HBO literature
b.) Oxygen delivered systemically at partial pressures lower than 1.4
ATA does not fulfill the criteria of bacteriostatic agents
(i.e., agents that suppress the growth and proliferation of bacteria;
(Park, M., 1999).

Park et al. (1999) reported
1.) Local environmental conditions permits the
proliferation of Pseudomonas aeruginosa.
2.) Topical oxygen does not augment the capacity of the
immune system
Topical Oxygenation enthusiasts
1.) Apparently aware (but perhaps unconcerned) by the
notable contradiction,
2.) Recommend , application of acetic acid when
problems wounds are Pseudomonas-positive,
Acetic Acid:
1.) Adjunctive topical acetic acid may act as an irritant

Mechanism of HBO
1.) Bactericidal effects of HBO YOU NEED free radicals by cells
of the immune system.
2.) THEREFORE, topical oxygen therapy would need to
augment free radicals.
3.) BUT, therapeutic free radical production is systemically
rather than locally medicated.
Conclude:
Basic premise upon which topical oxygen therapy is built is
false.

 Hyperbaric oxygen exerts its beneficial effects through
systemic rather than local actions.
1.) Zamboni et. al, (Zamboni, 1999). rendered the hindlimb
of rabbits ischemic for 8 hours, after which the flow of
blood was restored.
2.) Functional tests of the reperfused muscle revealed
beneficial effects of hyperbaric oxygen,
3.) Suggests that systemic factors contributed positively to
the recovery of function following reperfusion.
4.) Conducted in Humans

Topical oxygen
1.) What is the mechanism???? diminishing
reperfusion injury.
2.) Another assumption =
a.) Pure oxygen on a wound pure oxygen at
marginally elevated pressures would deliver
oxygen to the body at a rate similar to the lungs
receiving a load of pure oxygen at pressures
commonly in excess of 2 ATA.

Topical oxygen is non systemic
1.) Unable to have the beneficial suppression on
neutrophils which play a significant role in
reperfusion injury ( Zamboni et al)
2.) May play a detrimental role in conditions in
which ischemia is present

Basis of Evidence
1.) Heng MCY: Topical Hyperbaric Therapy for Problem Skin
Wounds. J Dermatol Surg.Oct 1975: 1:3:55-58
2.) Heng MCY, Kloss SG: Endothelial Cell Toxicity in Leg Ulcers
Treated with Topical Hyperbaric Oxygen. AM J Dermatopathol
1986; 8:403-410
3.) Leslie CA, Sapico FL, Ginunas VJ, Adkins RH: Randomized
Controlled Trial of Topical Hyperbaric Oxygen for Treatment of
Diabetic Foot Ulcers. Diabetes Care Feb 1988 11:2: 111-115.
Investigators reported tendencies for healing to decelerate in the
presence of topical

 Potential for oxygen to exert (potentially damaging)
effects in healthy tissue located far from the wound.
 Increase availability of cytotoxic free radicals.
 Therapeutically beneficial effects of hyperbaric oxygen
are achieved through the production of free radicals
(e.g., immune system-guided antibacterial effects).
Toxic effects of hyperbaric oxygen well documented
(Kindwall, E., 1999).
 A.) central nervous system,
 B.) lungs,
 C.) eyes,

1.) Dependent on the partial pressure of oxygen (Whelan et. al, 1999).
2.) central oxygen toxicity is a clinical concern at partial pressures of
oxygen greater than 2.0 ATA.
Manifestations
1.) Behavioral
2.) Dramatic seizures on EEG.
a.) overt signs (e.g., autonomic, affective, cognitive, or motor)
b.) Signs may be subtle or even absent,
c.) Progression between initial signs of central oxygen toxicity and
seizures may be rapid.


When?
1.) Partial pressures as low as 0.5 ATA
Symptoms
a.) Substernal burning,
b.) Chest tightness,
c.) Cough, and dyspnea,
d.) Likely reversible with the cessation of hyperbaric oxygen
therapy.
e.) IF not stopped = adult respiratory distress syndrome.
(Kobzik,1999).
Cases of irreversible pulmonary dysfunction have NOT
followed single-treatment hyperbaric oxygen protocols
such as those deployed by the United States Navy.

Diabetic and Elderly patients.
1.) Secondary to lenticular changes,
2.) Progressive myopia:
a.) Partial pressures of oxygen between 2.0 and 2.4 ATA
b.) Recurrent treatments lasting at least 90 minutes.
c.) 20 - 40% will experience visual changes.
The condition is reversible, typically resolving during
six treatment-free weeks.

 This condition is a rarity in the chamber,
 Most arrythmias usually improve within HBO
 Incidence < 0.2% ( Kindwall)
Case Report
1.) Individual suffered 30 cardiac arrests during the 48
hours he was treated during a research study.
2.) 28 of his 30 cardiac arrests occurred at the surface
The protocol
 Multiplace
> CPR can be immediatley initiated.
 Monoplace
>The patient must be removed from the chamber in
order to initiate cardiopulmonary resuscitation.

> This condition is a life threatening event
> If patien is decompressed it will increase as # ATA’s increase.
Signs of a pneumothorax
 SOB
 Chest pain,
 Tracheal deviation to the side of the collapsed lung
 Absence of breath sounds on the affected side.
Pathognomonic Test
 If the patients respiratory distress worsens on decompression and
improves immediately on recompression one can diagnose a
pneumothorax.
Treatment:
 The patient shoould be held at pressure until a management team can
be assembled, ( surgeon, anesthesiologist etc).
 The patient is then brought quickly to the surface
 A needle is place into the affected side to relieve pressure.

1.) Patients may be fitted with clear plastic hoods.
2.) Audio/visual entertainment systems may be
incorporated to add comforting distractions.
3.) Often fabricated from clear materials
4.) Afford visual contact between the patient and
the external Environment

1.) HBO therapy follows Physiological Principles and the Laws
of physics
2.) HBO is Currently indicated for 13 diseases and supported
by the literature
3.) Various “Fringe Therapy” based off of HBO
4.) Evidence includes testimonial and case reports
5.) THBO is a misnomer, that does not follow basic tenets of
certain physiological principles and laws
6.) THBO, is a therapy that physicians should be aware of and
not utilize

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Hinchliffe RJ , Valk GD , Apelqvist J , Armstrong DG , Bakker K , Game FL , et al . A
systematic review of the effectiveness of interventions to enhance the healing of chronic
ulcers of the foot in diabetes . Diabet Metab Res Rev 2008 ; 24 ( Suppl 1): 119 – 144.
 Whereas the systematic review of the International
Working Group that considered HBO accepted
that there was some evidence to support its use, it
is clear that more data are required from larger
controlled trials not only to confirm efficacy but
also to clarify which wounds might best benefit
from this expensive treatment

Bollero D, et al. THE ROLE OF NEGATIVE PRESSURE WOUND THERAPY IN THE
SPECTRUM OF WOUND HEALING. Ostomy Wound Management. 2010;56(5 Suppl):1–18.

 A number of growth factors and other agents
designed to modify abnormalities of the
biochemistry of the wound bed or surrounding
tissues have been described, but there is still no
consensus as their place in day - to - day
clinical practice. One example is platelet -
derived growth factor (PDGF) which is
available for clinical use in a number of
countries.
Jeffcoate WJ , Lipsky BA , Berendt AR , Cavanagh PR , Bus SA , Peters EJ , et al . Unresolved
issues in the management of ulcers of the foot in diabetes . Diabet Med 2008 ; 25 : 1380 – 1389 .

 Whereas there is some support for their use for
randomized clinical studies, their expense
together with the fact that most neuropathic
ulcers can be healed with appropriate
offloading, have limited their use.
Unfortunately, PDGF together with other
topically applied agents such as epidermal
growth factor do not have sufficient robust
 data to support their day - to - day use in
routine clinical practice.
Wieman TJ , Smiell JM , Yachin S . Efficacy and safety of a topical gel formulation of
recombinant human platelet - derived growth factor - BB (Becaplermin) in patients with chronic
neuropathic diabetic foot ulcers. Diabetes Care 1998 ; 21 : 822 – 827 .

 Similar to other treatments in this group of
adjunctive therapies although there is some
evidence to support the use of bioengineered
skin substitutes in non - infected neuropathic
ulcers, its use of somewhat restricted by cost. A
systematic review on this topic concluded that
the trials assessed were of questionable quality
and until high quality studies were performed,
recommendations for the use of these skin
substitutes could not be Made.
Blozik E , Scherer M . Skin replacement therapies for diabetic foot ulcers: systematic review
and meta - analysis . Diabetes Care 2008; 31 : 693 – 694 .

27 HBO Treatments / 6 ½ Weeks

Infected Calcaneous
s/p ORIF then
external fixation
Options: BKA vs HBO
25 yo Diabetic,
Standing on two
Feet changing oil.

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