Top INDEX
• Article:    Hyperbaric Oxygen Therapy : Current Trends and Applications.
• Policy:     Hyperbaric Oxygen Therapy indications, Contraindications & Complications.
• Report:    Hyperbaric Oxygen Therapy in Acute Ischemic Stroke: Results ...
• Report:    Hyperbaric Oxygen Therapy for Non-Healing Ulcers in Diabetes Mellitus.
• Brochure: Patient Education, Hyperbaric Oxygen Therapy.
• Article:    Hyperbaric Oxygen Therapy: Don't Be Misled.
• Report:    Hyperbaric oxygen therapy (1.5 ATA) in treating sports related TBI/CTE.
• Chart :     Hyberbaric Oxygen, ICU patient readiness.

  Comment: Supply of resting total O2 requirement.

  Comment: Range of Inconsistencies in data available.

  Comment: Changes in surrounding media pressure.

  -Focus-: Monographs on Toxins and Enhancers.

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Article: Hyperbaric Oxygen Therapy : Current Trends and Applications.
T Sahni: Consulant Internal and Hyperbaric Medicine, Indraprastha Apollo Hospital,
Sarita Vihar, New Delhi -- P Singh: Classified Specialist, Aerospace Medicine --
MJ John: Officer in Charge & Classified Specialist, Marine Medicine,
Institute of Naval Medicine, Naval Hospital, Colaba, Mumbai
R-Hyperbaric Oxygen Therapy Current.pdf JAPI -- VOL. 51 -- MARCH 2003

Abstract
Hyperbaric medicine is the fascinating use of barometric pressure for delivering increased oxygen dissolved in plasma to body tissues. Hyperbaric oxygen therapy (HOT) or hyperbaric oxygen (HBO) involves intermittent inhalation of 100% oxygen under a pressure exceeding that of the atmosphere, that is greater than 1 atmosphere absolute (ATA). .. Acute traumatic wounds, crush injuries, burns, gas gangrene and compartment syndrome are indications where addition of hyperbaric oxygen may be life and limb saving. Patients who are suffering with non-healing ulcers, decubitus ulcers (bed sores) and all late sequelae of radiation therapy are also benefited with HBO therapy. Acute hearing loss and many neurological illnesses are also now known to possibly benefit from hyperbaric oxygen therapy. This article aims to give a brief overview of the rationale, existing trends and applications of this therapy.

(p 280)
... hyperbaric facilities now form an important part of many hospitals all over the world. In 1996 there were 259 hyperbaric facilities in USA and there has been an annual increase in the number of hyperbaric centers and increase in patients at the rate of 15 and 620 respectively. The number of patients treated annually had increased from 896 in 1971 to 12,047 in 1989.

Experiences with HBO therapy in India have been published in select journals with limited circulation6-8 but there has been no interdisciplinary recognition of hyperbaric medicine at a national level. Thus though sufficient evidence supports use of HBO in certain defined conditions, many patients go untreated because of the physicians unfamiliarity with recent research of HBO as therapy.

The usual arterial partial pressure of O2 is 100 mm Hg, Hb is 95% saturated and 100 ml of blood carries 19 ml of O2 in combination with Hb and 0.32 ml dissolved in plasma. If the inspired O2 concentration is increased to 100%, O2 combined with Hb can increase to a maximum of 20 ml when the Hb is 100% saturated and the amount of O2 dissolved in plasma may increase to 2.09 ml. During HBO in addition to the Hb which is 100% saturated the amount of O2 carried in solution will increase to 4.4 ml% at a pressure of 2 ATA to 6.8 ml % at 3 ATA which is almost sufficient to supply the resting total oxygen requirement of many tissues without a contribution from oxygen bound to hemoglobin Table 1. It is this increased oxygen in plasma which is responsible for most of the beneficial effects of hyperbaric oxygen.

Hyperoxygenation causes immune stimulation by restoring WBC function, enhanced phagocytic capabilities and neutrophil mediated killing of bacteria. HBO2 accelerates neo-vascularization in hypoxic areas by augmentation of fibroblastic activity which further promotes capillary growth. HBO causes vasoconstriction in normal tissues but with an over all increased delivery of oxygen due to the hyperoxygenation. This is the basis of use in reducing edema and tissue swelling. In cerebral edema this helps to reduce edema while maintaining hyperoxia. It also reduces the adherence of white cells to capillary walls and is useful in acute brain and spinal cord injury. HBO therapy is bactericidal for anaerobic organisms such as Clostridi welchii, and also inhibits the growth of aerobic bacteria at pressures greater than 1.3 ATA. HBO at 2.5 ATA reduces the half-life of carboxyhaemoglobin from 4 to 5 hours in subjects breathing room air to 20 minutes or less and is the treatment of choice in carbonmonoxide (CO), smoke inhalations and acute cyanide poisoning.

When used in standard protocols of pressures that do not exceed 3 ATA (300 kPa) and the length of treatment is less than 120 minutes, hyperbaric oxygen therapy is safe. Commonest side effect is pain in the ears (aural barotrauma) as a result of inability to equalize pressure on both sides of the tympanic membrane due to a blocked eustachian tube. Pneumothorax and air embolism are more dangerous complications due to tear in pulmonary vasculature due pressure changes but are rare. Other rare side effects are pulmonary and neurological oxygen toxicity (Paul Bert effect), retrolental fibroplasia and cataracts. Transient reversible myopia can also rarely occur after prolonged HBO therapy. Fire is a realistic hazard but preventable by strict safety procedures and the patient may be claustrophobic.

Rare instances of hypersensitivity to O2 are also documented. Oxygen toxicity can be prevented in most tissues by using five minutes air in the chamber for every 30 minutes of oxygen. This allows antioxidants to deal with free oxygen radicals formed during the hyperoxic period. A suggested carcinogenic effect of hyperbaric oxygen has not been substantiated in extensive studies. ..

Non-healing ulcers, problem wounds, compromised skin grafts and flaps : These wounds have the underlying problem of tissue hypoxia, with oxygen tension usually below 20 mmHg, and therefore more prone to infection. The elevation of oxygen tension by hyperbaric oxygen therapy has powerful effects on wound dynamics, by both enhancing leukocyte bactericidal activity and promoting the fibroblast-collagen support needed for neovascularization. ..

Clostridial myonecrosis (Gas gangrene) :
Clostridium welchii cannot produce alpha-toxin when the patient undergoes HBO therapy.
The organism is not killed by hyperbaric oxygen and alpha-toxin is not detoxified by HBO, however, with production shut-off, alpha-toxin is fixed in the tissues within 30 minutes. It also has antibiotic synergeism with aminoglycosides, quinolones, sulpha and amphotericin B. A three-pronged approach consisting of HBO, surgery, and antibiotics is essential in treating gas gangrene.

Necrotizing soft tissue infections :
Hyperbaric oxygen therapy may be used as an adjunct treatment of soft tissue infections with tissue necrosis, due to mixed aerobic and anaerobic organisms. Increasing tissue oxygen tension enhances white cell killing of bacteria, promotes inhibition of anaerobic organism growth, and increases the oxidation-reduction potential. These conditions include necrotizing cellulitis, progressive dermal gangrene, anaerobic streptococcal myositis, crepitant anaerobic cellulitis, and necrotizing fasciitis. Primary management remains adequate surgical debridement and antibiotic coverage. The high mortality and morbidity with these conditions warrant the addition of adjunctive hyperbaric oxygen therapy.

Treatment of late radiation tissue damage (osteoradionecrosis, radiation cystitis, enteritis, etc.) : In a patient who has had between 2,000 and 5,000 rads, there is a possibility that there may be difficulties with subsequent healing. Above 5,000 rads, healing of any subsequent surgical wound will be a definite problem. HBO therapy remains the keystone of treatment of radiation-induced illnesses. Recently, a clearer understanding of its pathophysiology has evolved. The basic physiology of this process is a progressive obliterative endarteritis with resultant hypoxia and tissue ischemia. Hyperbaric oxygen induces neovascularization of tissue and the tissue PO2 rises to 81% of normal plus or minus 5% between 18 and 30 hyperbaric treatments. Successful surgery and grafting is possible with a PO2 of 75% of normal.

Controlled clinical experience has demonstrated a perioperative staging of hyperbaric oxygenation, termed the "Marx Protocol", has significantly reduced the incidence of post-operative infection, dehiscence, and healing delays. Two reports have specifically addressed the issue of hyperbaric oxygen's cost effectiveness in this disorder: Marx and colleagues and Dempsey et al. The authors concluded that in carefully selected patients, managed along algorithmic lines, the addition of hyperbaric oxygen therapy resulted in improved clinical outcomes while greatly reducing the overall cost. The effect of hyperbaric oxygen in radiation-induced bone necrosis, severe laryngeal necrosis, hemorrhagic radiation cystitis, colitis, scleral necrosis is also now well recognised. The cure rate for radionecrosis of the mandible now approaches 94% in those patients treated with hyperbaric oxygen.

Thermal Burns :
The burn is a complex and dynamic pathophysiologic process characterized by a zone of coagulation, surrounded by a region of stasis, bounded by an area of hyperemia. A significant body of data clearly supports the efficacy of hyperbaric oxygen in the treatment of thermal injury. Reduction in fluids, less conversion to full thickness injury, preservation of marginally viable tissue, improved microcirculation, reduction in edema, faster epithelialization, less inflammatory response, enhancement of PMN killing, preservation of tissue creatine phosphate, adenosine triphosphate and decreased wound lactate have all been reported with HBO. A significant reduction in hospital stay and cost of treatment with adjunctive hyperbaric oxygen therapy has been reported.

Neurological indications :
The rationale of use of hyperbaric oxygen in neurological indications is based on the finding in SPECT studies that around the central area of neuronal death is the penumbra: peri-infarct zone. This zone has hibernating/idling or sleeping neurons. Also what appears as gliosis (dead neurons) on CT scans may actually be viable tissue for years following the insult (confirmed with SPECT).24 HBO delivers high oxygen to these "sleeping cells" and reactivates them. HBO increases oxygen supply to the ischemic neurons, reduces edema and reverses the reduced flexibility of erythrocytes. This is the basis of its use by some centres in acute stroke, post-traumatic brain injuries and cerebral palsy. These studies have shown improvement in these indications. ...

Policy : Hyperbaric Oxygen Therapy indications, Contraindications and Complications.
HyperOxy-contraindications.pdf

This policy lists accepted conditions or indications for insurance reimbursement for Hyperbaric oxygen therapy (HBOT), contraindications and relative contraindications, and complications that may occur with and/or during HBOT. Additional information is provided regarding drug therapy with HBOT.

1.0 HYPERBARIC OXYGEN THERAPY (HBOT) ACCEPTED CONDITIONS FOR
INSURANCE REIMBURSEMENT:

1.1 The following list includes the currently accepted conditions:
     A. Air or gas embolism
     B. Carbon monoxide/cyanide poisoning and smoke inhalation
     C. Crush injury/traumatic ischemia
     D. Decompression sickness
     E. Enhancement in healing in selected problem wounds
     F. Exceptional anemia resulting for blood loss
     G. Gas Gangrene(clostridial)
     H. Necrotizing soft tissue infections
     I. Refractory osteomyelitis
     J. Comprised skin grafts/flaps
     K. Radiation tissue damage
     L. Thermal burns

2.0 ABSOLUTE CONTRAINDICATIONS

     2.1 Untreated pneumothorax
          A. Surgical relief of the pneumothorax before the HBOT treatment, 
               if possible, removes the obstacle to treatment.

3.0 RELATIVE CONTRAINDICATIONS--

"Conditions in which caution must sometimes be observed but 
which are not necessarily a contraindication to HBOT." (Kindwall, 1995)
3.1 History of spontaneous pneumothorax
3.2 Severe sinus infection
3.3 Upper respiratory infection
3.4 Asymptomatic pulmonary lesions on chest x-ray
3.5 Uncontrollable high fever (greater than 39C)
3.6 History of chest or ear surgery
3.7 Congenital spherocytosis
3.8 Any anemia or blood disorder (Although HBOT treats different types of anemia.)
3.9 Any convulsive disorder 
(Although many patients have seizure disorder and are treated successfully with HBOT.)

3.10 History of optic neuritis or sudden blindness
3.11 Middle ear infection
3.12 Diabetes mellitus (insulin therapy)
(Many diabetic wound patients are diabetic and are treated successfully with HBOT.)

3.13 Pregnancy
3.14 Nicotine use/addiction
3.15 Acute Hypoglycemia (Many patients are treated successfully with HBOT.)
3.16 Emphysema with CO2 retention 

4.0 POSSIBLE COMPLICATIONS

While important to consider, most patients do not experience the following:

4.1 Barotrauma 
(We've never had one of our patients experience barotraumas because we operate each dive manually, 
and at the first sign of pressure we can reverse the process and relieve any discomfort.)

4.2 Confinement Anxiety (Oxygen is a natural anti-anxiety for patients, and we have successfully
treated many patients with confinement anxiety in our extra large hyperbaric chambers.)

4.3 Oxygen toxicity (pulmonary and CNS) (1 in 10,000 people may experience this but no permanent
effects result from this occurrence. There are 14 signs that patients display before experiencing
oxygen toxicity that the CHT is trained to recognize. Once again, because we operate our chambers
manually, if a patient should start to display symptoms, the pressure is reversed and symptoms are
resolved.)

4.4 Myopia-Minor eyesight changes due to temporary curvature in the lens while undergoing slight
pressurization.

    A. Gradually reverses after cessation of HBOT when the lens flattens out again. 
       Patients report usually between 3 to 4 weeks.

    B. Resolved within three months in most cases (Jain, 1996)

5.0 THE USE OF DRUGS IN THE HYPERBARIC CHAMBER

5.1 "As A General Rule most drugs do not have any particular combined or synergistic effect with the compressed air or the increased oxygen partial pressure. Important exceptions exist. It is probably safe to assume that unless there are specific contraindications or precautions regarding use of a particular substance or compound under pressure it is safe to go ahead and administer it.-- (Kindwall, 1995)

5.2 No intramuscular injections are to be given immediately before or after each HBOT treatment as the intense constriction under pressure results in almost no drug absorption. Decreasing pressure (surfacing) would cause sudden drug absorption due to vasodilation. Injections are best administered 1 or 2 hours prior to or after each HBOT treatment.

5.3 Intravascular injection is not the route of choice for administering drugs.
The vasoconstrictive effective effect of HBOT causes a slow uptake.
At the completion of the treatment, patients could be susceptible top the effects of sudden release of the drug into circulation. Prior administration by mouth is preferable when possible.

6.0 DRUGS AFFECTING THE CENTRAL NERVOUS SYSTEM

6.1 Steroids and adrenaline may both cause an increased sensitivity to oxygen toxicity.

6.2 Narcotics may sensitize the patient to oxygen toxicity.

A. Narcotics depress respiration by decreasing medullary reactivity to CO2 and O2.

B. Hyperbaric Oxygen can cause a depression of respiration, especially in the presence of narcotic drugs.

C. The exaggerated depression of ventilation leads to an increased PCO, which in turn leads to vasodilatation in the brain blood vessels. The accompanying increased blood flow results in an increased amount of dissolved oxygen in the brain and may lead to oxygen convulsions. (Jain, 1996)

6.3 CNS Stimulants, such as amphetamines interact unfavorably with HBOT.

A. Diet Pills
B. Excessive coffee drinking in those susceptible to caffeine.

6.4 Scopolamine may be used concomitantly with HBOT; however, the visual and cardiovascular side effects of the drugs should be taken in consideration.

6.5 Carbonic anhydrase inhibitors tend to promote CO2 retention and vasodilatation.

A. Mafenide acetate (Sulfamylon), an antibacterial agent used in burn patients must be removed before treatment in the Hyperbaric chamber.

B. Acetazolamide is a carbonic anhydrase inhibitor which prevents oxygen induced vasoconstriction.
If a patient is taking acetazolaimide as a diuretic when referred for treatment, there will be a risk of oxygen seizure. It should not be used at pressure greater than 2 ATA.

7.0 INTERACTIONS WITH ISCELLANEOUS DRUGS

7.1 Digitalis - some evidence suggests that HBOT may reduce the toxic effects of digitalis.

7.2 Insulin dosage required for IDDM will be decreased during HBOT. Blood glucose levels should be monitored closely and dosage should be adjusted accordingly.

7.3 Reserpine (Serpalane) and guanethidine (Iselin), antihypertensive which decreased arterial, vasoconstriction, may have been shown to interact unfavorably with HBOT.

7.4 aminophylline causes an increase in gas bubbles due to shunting of gases across the lungs.

7.5 The use of Thyroxin or the excess production of the thyroid horine (as in Graves Disease) predisposes to oxygen toxicity. Thyroidectomy has the opposite effect.

7.6 Bleomycin, an antineoplastic, is known for pulmonary toxicity.

7.7 Doxorubicin (Adriamycin) and Cis-Platinum, angioplasties, are contraindicated.

7.8 Disulfiram (Antabuse) may potentiate oxygen toxicity.

8.0 DRUGS THAT PROTECT AGAINST OXYGEN TOXICITY

8.1 The drug should reach the right location at the right time, and remain effective there in the face of continuous hypoxia, without itself inducing any toxic effects. There is no such ideal drug available at present. However, the following provide some benefits (Jain, 1996)

A. Antioxidants, free radical scavengers and trace minerals.

     1) Allopurinol
     2) Ascorbic acid
     3) Magnesium
     4) Selenium
     5) Vitamin E- a daily dose of 400mg should be given starting two Days before the therapy.

B. Chlorpromazine (Thorazine)

C. Lithium

D. Levodopa

8.2 Anticonvulsants - if anticonvulsants are used prophylactically to suppress convulsions, it is critically important that the usual oxygen pressure/time limits be strictly observed. Suppression of convulsions is exposed is carried beyond the latent period for oxygen toxicity can occasion permanent oxygen damage to the CNS. In clinical exposures of no more than 90 minutes limited to 3 ATA, permanent damage has not been reported in the human. Drugs to protect against seizures include:

A. Diazepam
1) Seizures due to convulsive disorders (not due to Hyperbaric therapy).
2) Seizures due to oxygen toxicity, prophylaxis in patients with a high risk of oxygen toxicity.
Usually an increased dose of Diazepam is required in the hyperbaric environment (up to 30mg IV PRN has been used).

B. Lorazepam is similar to Diazepam, but requires one-fifth the dose.

C. Carbamazepine has been found to be useful for the prevention of CNS toxicity during HBOT of epilepsy-prone patients.

References:
Jain, K. (1996). Textbook of Hyperbaric medicine. Seattle: Hogrefe & Huber.
Kindwall, E. (1995). Hyperbaric Medicine procedures. Flagstaff, AZ: Best Publishing.

Report: Hyperbaric Oxygen Therapy in Acute Ischemic Stroke:
Results of the Hyperbaric Oxygen in Acute Ischemic Stroke Trial Pilot Study.
Daniel E. Rusyniak, Mark A. Kirk, Jason D. May, Louise W. Kao,
Edward J. Brizendine, Julie L. Welch, William H. Cordell and Robert J. Alonso
Stroke. 2003;34:571-574; originally published online January 16, 2003
http://stroke.ahajournals.org/content/34/2/571
http://stroke.ahajournals.org/ Stroke-2003-Rusyniak-571-4-OxygenTherapy.pdf

Hyperbaric oxygen therapy (HBO) represents a possible therapy for acute ischemic stroke.
Potential benefits include increased oxygen delivery, decreased cerebral edema, decreased lipid peroxidation, inhibition of leukocyte activation, and maintenance of blood-brain barrier integrity. HBO has been shown in animal models of both focal and global ischemia to reduce the volume of brain infarction and improve outcome.

There have been >400 cases of ischemic strokes in humans treated with HBO, with more than half of these cases claiming improvement on clinical or experimental grounds. Despite this result, there have been only 2 controlled pilot studies in humans, both using multiple treatments at 1.5-atm pressure absolute (ATA).

...

There are several possible explanations for the results presented here.
Patients with ischemic stroke may have a narrow therapeutic time window in which HBO is beneficial. In our study, patients were treated within 24 hours of symptom onset, with only 15% of them receiving treatment within 6 hours of symptom onset. In animal models of ischemic stroke, Weinstein et al showed that the benefit conferred by HBO was lost in those animals treated less than 4 hours after artery occlusion. In the 2 prior human studies of HBO for stroke, the average times to treatment were 51.8 and 18 hours. Neither of these studies demonstrated any benefit, although the study by Nighoghossian et al1 did show a trend toward benefit in the HBO group at 1 year.

Other explanations may be that the pressure used in this study was too high.
Although data exist suggesting that patients with primarily traumatic brain lesions had impaired glucose utilization at pressures of 2.0 ATA compared with 1.5 ATA,16 we chose 2.5 ATA on the basis of animal data showing decreased lipid peroxidation, decreased leukocyte activation,4 and improved integrity of the blood-brain barrier5; animal studies have shown that treatment pressures of 2.5 ATA result in improved outcome and smaller infarctions. Because HBO has been shown to increase free radical formation in the rat brain, it is possible that it may contribute to worsening reperfusion injury. Animal studies, however, have shown that HBO did not increase brain lipid peroxidation, a byproduct of free radicals interaction with neuron membrane phospholipid. ...

Report: Hyperbaric Oxygen Therapy for Non-Healing Ulcers in Diabetes Mellitus.
Hyperbaric Oxygen Therapy - Ontario Health Technology Assessment Series 2005; Vol. 5, No. 11
http://www.health.gov.on.ca/ohtas ... rev_hypox_081105.pdf

The Medical Advisory Secretariat
Ministry of Health and Long-Term Care
20 Dundas Street West, 10th floor
Toronto, Ontario
CANADA
M5G 2N6
Email: MASinfo@moh.gov.on.ca
Telephone: 416-314-1092

(p 06) Diabetes mellitus is a chronic disease characterized by an increase in blood sugar that can lead to many severe conditions such as vision, cardiac, and vascular disorders. The prevalence of DM is difficult to estimate, because some people who have the condition are undiagnosed or may not be captured through data that reflect access to the health care system. The Canadian Diabetic Association estimates there are about 2 million people in Canada with diabetes (almost 7% of the population). According to recent data, the prevalence of DM increased from 4.72% of the population aged 20 years and over in 1995, to 6.19% of the population aged 20 years and over in 1999, or about 680,900 people in 1999. Prevalence estimates expanded to 700,000 in 2003. ..

Hyperbaric oxygen therapy has been in use for about 40 years.
It is thought to aid wound healing by supplying oxygen to the wound. According to the Hyperbaric Oxygen Therapy Association, HBOT acts as a bactericidal, stops toxin production, and promotes tissue growth to heal difficult wounds. During the procedure, a patient is placed in a compression chamber with increased pressure between 2.0 and 2.5 atmospheres absolute for 60 to 120 minutes, once or twice daily. In the chamber, the patient inhales 100% oxygen. Treatment usually runs for 15 to 20 sessions. ..

(p 11) Little is known about the wound-healing process, and this makes treating chronic wounds challenging. Usually, a DM foot ulcer takes between 12 and 20 weeks to heal. (4) Many therapies exist for treating wounds in persons with DM, such as: (4)

• Identification and correction of the etiological cause of the wound
  (e.g., ensuring good nutrition and maintaining normal blood glucose)

• Current best practices for the treatment of chronic wounds including debridement and infection control

• Preventive and therapeutic strategies such as orthopedic shoes/devices and shoe fitting to resist blisters and wounds, and off-loading to relieve pressure on the foot.

• Amputation in very severe cases.

(p 12) During the procedure, a patient is placed in a compression chamber with increased pressure between 2.0 and 2.5 atmospheres absolute (ATA) for 60 to 120 minutes, once or twice daily. In the chamber, the patient inhales 100% oxygen. Each treatment cycle consists of 15 to 20 treatment sessions.

(p 15) The literature search spanned 1966 to 2003 using the standard medical search databases (MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials) and DORCTHIM (a specialized hyperbaric medicine database); results were cross-referenced to the Cochrane Wounds Group Special Trials register. Six studies with 191 patients were included. Out of 6 RCTs included in the review, 5 focused on HBOT for non-healing wounds due to diabetes, and 4 focused on the outcomes of interest for the Medical Advisory Secretariat's health technology policy assessment. ..

(p 16) The authors also analyzed the cost of treating diabetic wounds. They found a cost savings of $63,100 (AU) or less per amputation avoided with the use of HBOT based on 15 to 40 sessions that cost $6,941 (AU). A caveat about these estimates, however, is that the conclusion of the effectiveness of HBOT was based on limited evidence.

(p 23)
Direct Costs of Hyperbaric Oxygen Therapy and Chronic Wounds

All costs are in Canadian currency. 
The cost to lease a hyperbaric oxygen chamber is about $275,000 
plus $315,000 in variable and fixed costs annually 
(e.g., maintenance, staff resources, medical supplies, etc.).

The cost of HBOT per treatment cycle for a patient that has DM and an ulcer 
is estimated at $5,200 based on 100 patients treated each year with 1 chamber (Personal communication, 2005),
plus amortization of the cost of the machine (about $1,000). 

Thus, the total cost per patient is about $6,200.

It is estimated that the hospital cost for a patient that has DM and an ulcer, 
and that does not require amputation, is $58,500 (based on 78 days in the hospital at $750 per day). 
The estimated system cost for an amputation is $60,000 per patient (Personal communication, 2005).

To determine the possible cost avoidance of HBOT, the following analysis was done:
 -- Cost avoidance for 1 amputation: $ 60,000 (cost amputation) - $6,200 (HBOT) = $53,800


Cost avoidance in Ontario:

    Low estimate: One-third of amputations avoided with HBOT (Cochrane estimate)
    357 major amputations in Ontario x 0.30 = 107.1 x $53,800 = $5.8 million

    High estimate: 
    All amputations avoided with HBOT 357 major amputations in Ontario x $53,800 = $19.6 million

Thus, between $5.8 million and $19.6 million in costs could be avoided based on current estimates 
if HBOT was deemed effective at preventing amputations in patients who have DM and foot ulcers.

(p 24) There are about 700,000 people in Ontario with diabetes, and 10% to 15% of these people may have a foot ulcer sometime in their lives. Foot ulcers are treatable when they are identified, diagnosed, and treated early, according to best-practice guidelines. Routine follow-up for people with diabetes who may be at risk for neuropathy and/or peripheral vascular disease may prevent subsequent foot ulcers. HBOT is an insured service in Ontario; however, fewer than 20 people with DM were treated with this herapy in 2003, according to hospital discharge abstracts. There are 3 centres housing 6 hyperbaric oxygen chambers in Ontario.

Brochure: Patient Education, Hyperbaric Oxygen Therapy.
A guide to help you learn about and get ready for your treatment.
Hamilton Health Sciences
Hamilton General Hospital
PD 4885 -- 07/2003
dpc/pted/pamp/HyperbaricPORTRAIT-trh.doc
dt/July 14, 2003

Hyperbaric oxygen therapy is a painless treatment that increases the amount of oxygen in your body. This is done by breathing pure oxygen while you are in a hyperbaric oxygen chamber.

A hyperbaric oxygen chamber is an enclosed chamber that you lie inside. The pressure inside the chamber is increased as you breathe pure oxygen.

The increased pressure inside the chamber allows your tissues to take up more oxygen. More oxygen into your tissues helps your body heal faster by speeding up the formation of new tissue and fighting infection.

The chamber is a clear tube so you will be able to see through it. The therapist will always be in the room and you will be able to see and talk to the therapist. You will be able to see the chamber before your first hyperbaric oxygen treatment. ...

How do I get ready to go in the hyperbaric chamber? Before you start your treatment:

• go to the bathroom
• remove your underwear, nylons and socks
• put on the special gown
  You cannot wear:
  • contact lenses, dentures, and/or hearing aids
  • jewellry
  • hair spray
  • ointments
  • makeup
  • creams
  • nail polish
  • perfume or cologne
  • lotions or petroleum jelly
  • deodorant
  • velcro
  • watch
  • hair elastic bands
  • You cannot chew gum or suck candies in the chamber.
  • You can wear your eyeglasses.
  • We will give you a bottle of water to drink and
  • a bed pan to use in the chamber if needed.

    Sorry, books and magazines are not allowed inside the chamber.
    However, a television is available for viewing and you can hear the sound inside the chamber.

You will be given a special gown to wear during your treatment.
It is made of 100% cotton to reduce the risk of static electricity.
Please do not wear any other clothing underneath the gown.
Check with the therapist if you are not sure.

If you have a wound dressing on, please check with the therapist to see if it is all right to wear it during your treatment.

Do not drink anything carbonated such as CokeTM within 1 hour to the start of your treatment as this could cause stomach pain.

Avoid food and drinks with caffeine too.

Do not smoke during the course of your treatment.
Smoking reduces the amount of oxygen your blood can carry and will reduce the effectiveness of the treatment.

If you drink alcohol, please discuss this with the doctor.
Drinking alcohol during your treatment course could cause a seizure.

If you have diabetes, please tell the therapist your morning blood sugar result and eat a normal breakfast.

Tell the therapist if you did not sleep through the night before your treatment.

How long does each treatment last?
A typical treatment lasts between 2 to 2 1/2 hours.
The number of treatments you will need depends on why you are having hyperbaric oxygen therapy.
Your doctor will discuss your treatment schedule before it starts.

What will I feel during the hyperbaric oxygen treatment?
As the chamber is pressurized, you may feel a rise in the temperature.
You will hear the oxygen coming into the chamber.
It may sound like hissing or a waterfall.
You will feel a fullness in your ears as your eardrum is exposed to the pressure change.
This feeling is similar to that felt in an airplane.
The therapist will teach you how to deal with this.
Never allow your eardrums to become painful.
Always tell the therapist if you are having problems adjusting to the pressure change.

Let the therapist know if you:
1. feel nauseous
2. have tingling in your face
3. 2 see double

What are the side effects?
Some side effects include nausea, earache, and vision changes during your treatment.
Do not change your eyeglass prescription since the vision changes are temporary and your vision will return to normal.

Why is my wound painful? The treatment is causing an increase in the flow of blood to the wound.
This may increase the pain but is a sign of the healing process.

Article: Hyperbaric Oxygen Therapy: Don't Be Misled.
FDA Consumer Health Information / U.S. Food and Drug Administration AUGUST 2013

No, hyperbaric oxygen therapy (HBOT) has not been clinically proven to cure or be effective in the treatment of cancer, autism, or diabetes. But do a quick search on the Internet, and you'll see all kinds of claims for these and other diseases for which the device has not been cleared or approved by FDA. ...

"Patients may incorrectly believe that these devices have been proven safe and effective for uses not cleared by FDA, which may cause them to delay or forgo proven medical therapies," says Nayan Patel, a biomedical engineer in FDA's Anesthesiology Devices Branch. "In doing so, they may experience a lack of improvement and/or worsening of their existing condition(s)." ...

HBOT involves breathing oxygen in a pressurized chamber in which the atmospheric pressure is raised up to three times higher than normal. Under these conditions, your lungs can gather up to three times more oxygen than would be possible breathing oxygen at normal air pressure.

Patel explains that your body's tissues need an adequate supply of oxygen to function. When tissue is injured, it may require more oxygen to heal. "Hyperbaric oxygen therapy increases the amount of oxygen dissolved in your blood," says Patel. An increase in blood oxygen may improve oxygen delivery for vital tissue function to help fight infection or minimize injury.

Thirteen uses of a hyperbaric chamber for HBOT have been cleared by FDA.
They include

1. treatment of air or gas embolism (dangerous "bubbles" in the bloodstream that obstruct circulation),
2. carbon monoxide poisoning,
3. decompression sickness (often known by divers as "the bends"), and
4. thermal burns (caused by heat or fire).

Report: Hyperbaric oxygen therapy (1.5 ATA) in treating sports related TBI/CTE.
Stoller Medical Gas Research 2011, 1:17
http://www.medicalgasresearch.com/content/1/1/17 (5 July 2011)
Medical-Gas-Research--2045-9912-1-17.pdf

Abstract Despite adequate evidence, including randomized controlled trials; hyperbaric oxygen is not yet recognized as efficacious for treating various forms of brain injury, specifically traumatic brain injury. Political-economic issues have kept this benign therapy from being widely adopted despite the lack of viable alternatives. Two football players with TBI/CTE are herewith shown to benefit from being treated with hyperbaric oxygen as documented by neurocognitive examinations and functional brain imaging, in one case treatment commenced decades after the brain injury. Perhaps the interest in HBOT by those participating in high-risk sports will help expand this orphan therapy into mainstream medicine.

Many more concussions were being reported in the National Football League (NFL) in the 2010 season.
A total of 154 concussions, including practices and games, were reported from the start of the preseason through the eighth week of the 2010 regular season. That is an increase of 21 percent over the 127 concussions during the same span in 2009, and a 34 percent jump from the 115 reported through the eighth week of the 2008 season. (Associated Press, Dec 13, 2010) This either means better reporting is taking place or the game is getting more violent or some combination of the above. What hasn't changed is a lack of treatment. ...

HBOT has been treating brain injuries as far back as 1963, when it was first found effective in treating carbon monoxide poisoning [1,2]. Although the misconception that HBOT is only treating carboxy-hemoglobin persists to this day [3]. Brain injuries caused by decompression sickness and arterial gas emboli began being treated by HBOT using Navy Treatment Table six [4,5]. Delayed treatment (3 months) of an ischemic stroke with HBOT was reported by the US Navy in 1969 [6]. Subsequently successful treatment with HBOT for late treatment of a stroke, diabetic encephalopathy and near-drowning/global anoxia was also reported [7] with the additional evi- dence of pre and post functional brain imaging (SPECT).

The medical literature continues to grow showing HBOT is efficacious in treated old carbon monoxide poisoning (COP) also known as delayed neuropsychiatric syndrome (DNS) of COP [8,9].

While the historic literature points to HBOT as being efficacious for many conditions, HBOT is an orphan ther- apy that falls outside of the medical paradigm where drugs and interventions are selectively fed into the standard-of-care/reimbursement complex by corporate interests that control both medical information and clinical practice trends. A therapy that exists outside our dysfunctional medical paradigm tends to be but a footnote that is passed over, buried or ignored completely.

Despite controlled randomized trials demonstrating HBOT's efficacy for treating TBI, ignoring HBOT for treating brain injuries seems to have became codified even though other forms of intervention have fallen short. High quality clinical trials demonstrating the efficacy of HBOT in brain injury eventually get buried or forgotten. Sometimes, those who don't understand the nuance of oxygen dose or timing perform studies and resulting misinterpreted results further marginalize this important tool for treating brain injury [10].

While in acute severe TBI, HBOT has been shown to be effective in reducing mortality,[11] Harch et al. demonstrated consistent SPECT brain imaging improvements (showing improved brain blood flow) in chronic TBI patients treated with HBOT 1.5 [12-15]. Since the original work of Drs. Neubauer and Harch, the efficacy of HBOT 1.5 in a chronic stable TBI has been well documented [16,17]. Patients with abnormal functional brain scans secondary to TBI show consistent improvement after HBOT 1.5. ...

HBOT is the only non-hormonal treatment approved by the FDA for the repair and regeneration of human tissue. Six of the 13 approved indications are directly related to brain injury and wound repair relevant to treating TBI. ... this benign, humanitarian and non-invasive therapy is recognized as a quintessential tool for treating brain injury; after all, oxygen is what the brain fundamentally feeds upon. ...

Abbreviations
ATA: atmospheres absolute; COP: carbon monoxide poisoning; CTE: chronic traumatic encephalopathy; DNS: delayed neuropsychiatric syndrome; HBOT: hyperbaric oxygen therapy; IMPACT: immediate post-concussion assessment and cognitive testing; NFL: National Football League; PCS: post concussion syndrome; SPECT: single-photon emission computed tomography; TBI: traumatic brain injury.

Chart : Hyberbaric Oxygen, ICU patient readiness.
hyperbaric-oxygen.pdf

Hyperoxygenation Influences:
• Angiogenesis in ischemic tissues
• Bacteriostatic/bacteriocidal actions
• Carboxyhemoglobin dissociation hastened
• Clostridium perfingens atoxin synthesis ingibited
• Phagocytic bacterial killing improved
• Temporary inhibition of neutrophil B2 integrin adhesion
• Vasoconstriction

Health Conditions that often Benefit:
• Air or gas embolism
• Carbon monoxide poisoning
• Clostridial myositosis and myonecrosis
• Crush injury, compartment syndrome, acute traumatic ischemia
• Decompression sickness
• Enhancement of healing in selected wounds
• Exceptional blood loss anemia
• Necrotizing fascitis
• Chronic refractory osteomyelitis
• Radiation necrosis
• Thermal burns

Monitoring & equipment issues
1. The patient is attached to equipment at ambient pressure before treatment, and once the treatment pressure is achieved all settings are checked and transducers recalibrated.

2. Among the items that must be checked is the cuff pressure of endotracheal tubes. The usual practice is to replace the air in these cuffs with an equivalent volume of sterile saline before treatment to avoid volume changes related to pressurization.

3. If glass bottles, pressure bags, or any other gas-filled equipment are used inside a hyperbaric chamber, they must be adequately vented and closely monitored during a treatment.

Middle ear barotrauma
- Middle ear barotrauma is the most common adverse effect of HBO2 treatment

- Standard protocols include instruction of patients on autoinsufflation techniques and adding oral or topical decongestants when needed. When autoinsufflation fails, tympanostomy tubes must be placed.

CNS toxicity:
• CNS O2 toxicity is manifested as a grand mal seizure.
  This occurs at an incidence of approximately 1 to 4 in 10,000 patient treatments.
  The risk is higher in hypercapnic patients, and possibly those who are acidotic or with compromise due to sepsis, because an incidence of 7% (23 in 322 patients) was reported in case series of HBO2 treatment of gas gangrene.

• Seizures are relatively easy to manage in most cases:
  simply reduce the inspired O2 tension while leaving the patient at the same ambient pressure (to avoid pulmonary overexpansion injury when a patient is in tonic convulsion phase).

Ocular toxicity:
- Progressive myopia has been reported in patients who undergo prolonged daily therapy, but this typically reverses within 6 weeks after termination of treatments.

- Development of nuclear cataracts has been reported with excessive treatments that exceed a total of 150 to 200 hours, and the change does not spontaneously reverse.

Process:

HBO2 treatment is carried out in either a monoplace (single person) or multiplace (typically 2 to 14 patients) chamber.

Pressures applied while in the chamber are usually 2 to 3 atmospheres absolute (ATA), the sum of the atmospheric pressure plus additional hydrostatic pressure equivalent to one or two atmospheres.

Treatments usually are for 2 to 8 hours, depending on the indication, and may be performed from one to three times daily.

Monoplace chambers are usually compressed with pure oxygen.

Multiplace chambers are pressurized with air, and patients breathe pure oxygen through a tight-fitting facemask, a hood, or endotracheal tube.

During treatment, the PaO2 typically exceeds 2000 mm Hg and levels of 200 to 400 mm Hg occur in tissues.