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The content and information provided within this site is for informational and educational purposes only. Consult a doctor before pursuing any form of therapy, including Hyperbaric Oxygen Therapy. The Information provided within this site is not to be considered Medical Advice. In Full Support of the F.D.A., Hyperbaric Oxygen Therapy is considered Investigational, Experimental, or Off Label.

Please consult with your Treating Medical Physician

These questions are answered by the experts in the field of Hyperbaric Oxygen Therapy from around the world.

Not intended as medical advice, Please check with your treating Physician: See section "Suggested Reading".

Traumatic Brain Injury

When you approach physicians about using more oxygen in traumatic brain injury, give them references:

1-Sukoff MH, Ragatz RE. Hyperbaric oxygenation for the treatment of acute cerebral edema. Neurosurgery 1982;10:29-38.

2- Rockswold GL, Ford SE, Anderson DC, et al. Results of a prospective randomized trial for treatment of severely brain-injured patients with hyperbaric oxygenation. J Neurosurg 1992;76:929-934.

3-Neubauer RA, Gottlieb SF, Pevsner NH. Hyperbaric oxygen treatment for closed head injury. Southern Med J 1994;87:933-936.

Continuing evolution of brain damage over 22 years, the reference is;

4-Courville CB, Kimball TS. Histologic observations in a case of old gunshot wound of the brain. Arch Path 1934;17: 10-21.


Q: Can HBO2 help the nervous system?

Answer: A paper describes tissue oxygen tensions in the nervous system when oxygen is administered. This is essential reading for anyone involved in hyperbaric medicine. The work was undertaken in the Bowman Gray School of Medicine Winston Salem N Carolina USA. Reference: Kelly DL et al. Effects of hyperbaric oxygenation and tissue oxygen studies in experimental paraplegia. Neurosurgery 1972;36:425-429.

Q: Could HBO2 help nervous system damage in newborns?

Answer: The development of the myelin sheaths, which form the white of white matter by covering the nerve fibers normally, begins at about two weeks before term. The process begins in the spinal cord and proceeds towards the newest areas of the brain to develop - the frontal lobes of the hemispheres - being complete by about the age of 2. The blood vessels of the brain undergo dramatic changes in the last 2 weeks in utero in preparation for birth. If a child is born prematurely the brain, may not be able to deal with the period of oxygen deficiency during delivery - in the change from placental to lung oxygen transfer. As a result, there is development of edema and as a consequence oxygen deficiency (hypoxia) in the mid brain. The damage prevents the migration of the oligodendrocytes, which form myelin forward from the brain stem, and so the white matter does not develop. The extent to which this process can be ameliorated depends on the degree of damage - in the most severely affected children; this area of the brain undergoes cystic degeneration. There is a great deal of research being undertaken into remyelination for patients with multiple sclerosis and so there is some reason to hope that one day a therapy may be able to help. A course of oxygen therapy may produce some small changes that may improve your son's quality of life.

Philip James, M.D.

Reprinted with Permission


Q: How does oxygen help multiple sclerosis patients?

Answer: Multiple sclerosis is a disease in which there are multiple areas of leakage from the blood vessels in the brain and spinal cord causing symptoms. Treatment should be instituted when the first area is affected, but this is not yet an objective in neurology. Vessels in the nervous system are engineered to form a barrier - the blood-brain barrier - to prevent the leakage of large molecules such as proteins because their escape causes inflammation. The blood vessels involved in MS are actually veins and the leakage causes inflammation in the surrounding area. This is usually in the white matter, which contains vulnerable cells, which form the myelin sheaths. As the damage, progresses the sheaths are removed and the fibers are destroyed causing disability. Further progression is characterized by loss of the structure of the tissue and healing by scarring - known as sclerosis. Once the sclerosis has formed, recovery of the normal architecture is not possible. The key to the successful management of the established disease is to give the normal recovery mechanisms the best environment to repair the tissue before scarring takes place.

Magnetic resonance scanning techniques have shown both the leakage and the oxygen deficiency created by the swelling in the areas affected in MS. The object of giving a concentrated dose of oxygen is to restore the level of oxygen in the affected area to normal and interrupt the progression to scar formation. Oxygen is necessary, not only for all metabolism, but also for the regulation of many aspects of blood vessel and blood cell function. The blood-brain barrier requires energy and oxygen to maintain its integrity. Giving more oxygen constricts the diameter of blood vessels and yet paradoxically improves the transport of oxygen to the tissues. Oxygen also modulates the behavior of white blood cells and the inner lining of the vessels. Trials of oxygen therapy in MS patients have shown benefit especially in bladder function and balance but, because neurologists have wanted to avoid the possibility of spontaneous improvement - which is of course oxygen dependent - they have chosen to study patients who have advanced disability. Most trials have used patients with disease durations typically in excess of two years. The only trial in the history of multiple sclerosis, which matched pairs of patients and then randomly allocated them to either treated or control groups, demonstrated unequivocal evidence of benefit. (P< 0.0001). Because the blood vessel barrier may not repair completely, many patients need to continue oxygen therapy on a regular basis. This is also the reason for the need to continue with beta interferon injections, which also acts by stabilizing the blood-brain barrier.

Reference Fischer BH et al. Hyperbaric oxygen in the treatment of multiple sclerosis; a randomized placebo-controlled double-blind trial. New England Journal of Medicine 1983;308:181-186.

Dr. Philip James

Reprinted with Permission


Head injury and closed minds

To parents, patients and caregivers on the list: Those wanting to find out more about oxygen treatment will be disappointed that some professionals do not appear to be open minded. A head injury may close the mind, but hyperbaric oxygenation has been shown in a controlled trial to reduce the mortality of head injury by 50%. (Rockswold GL et al J Neurosurg 1992;76:920-34) Determine the knowledge of this therapy of a health professional by first asking if they know this paper. If they do not then move on. If they do then ask: Is the reduced mortality with the use of HBOT in head injury because blood flow is reduced or increased? Answers?

Best wishes,

Philip James,
Dr P.B. James MB ChB DIH PhD FFOM,
Wolfson Hyperbaric Medicine Unit
University of Dundee

Reprinted with Permission


Q: What stands in the way of using oxygen for neurological treatment?


Few months ago, I finally rented an Academy-award winning movie entitled "Lorenzo's Oil". I believe every parent should watch it because it's like watching us. Sadly, even if there were half a dozen double-blind controlled studies that proved HBOT efficacy for brain-injured children--I don't think pediatric neurologists would prescribe it. I'm not kidding. Go watch that movie. If an answer came from someone other than a board-certified neurologist, they won't have anything to do with it. Lorenzo's oil works, but pediatric neurologists don't ever prescribe it.

The same thing occurs with HBO2. That's why I believe making HBO2 a LEGAL RIGHT will finally empower parents and other caregivers to force the neurology community to be accountable. Right now, they are not--and never have been--because "the brain is a mystery" and they're holding a worthless piece of paper that credentials them to be "the experts". The worthlessness of that piece of paper became official in Georgia on October 10, 2001. The judge ruled that pediatric neurologists know nothing about repairing brain-injury. The judge even said that pediatric neurology is not even interested in the repair of brain-injury and therefore their opinion of HBO2 is irrelevant. it looks like every brain disorder has some sort of deficit in the area of cerebral blood flow. Everything. Now, if cerebral palsy stems from lack of complete cerebral blood flow and hyperbaric oxygen can restore that circulation, why couldn't the same be true for any and every brain disorder that stems from insufficient cerebral blood flow? I think that's a very legitimate question. Legitimate in light of the fact that long-term, chronic neurological disorders bring all kinds of secondary problems: spasticity, reflux and other eating disorders, mobility problems, continence problems and so forth. As a result, just one brain-injured person can keep a lot of people working for a long time. In addition, if that one brain-injured person can have the symptoms of his problem either masked or controlled through pharmacologics, that one brain-injured person is a 20-40-year customer. Fix the disorder (restore the cerebral blood flow), and you lose a lifelong customer.

Thank you,
D.F. in Georgia

Reprinted with Permission


Q: Why are HBO2 treatment outcomes for stroke or other brain injuries so varied?

Answer: The ultimate clinical status and recovery with brain injuries depend upon: the size and location of the epicenter or core of irreversible destruction; the surrounding zone of dormant but recoverable neurons (ischemic penumbra) fanning out in varying rings from the center core; the asymmetry involved; the reorganization and plasticity of altered and no impaired sensory and motor brain functions; meshing of sensory and motor fibers at the brain stem cord junction; progression of temporal intervention with HBO2

Dr Philip James MD

Reprinted with Permission

Here is a letter from someone who has first hand experience with stroke treated using increased pressure oxygen: Hello Michael, We finally got a link set up on our website. My sister Susan Reimer has been in talks with Sue Rodriguez of Rapid Recovery and asked theirs to be linked as well. Not only does our web developer have brittle diabetes but last week suffered a stroke at 3 AM, went to the hospital in the morning and came to our clinic at 2 PM same day. He walked very unsteady, talked with a "thick tongue" and had facial line irregularities. When I attended to him in the chamber, he tried to verbalize about how quickly life can be taken from you and that he never thought this would have happened to him despite his diabetes. I comforted him by saying that I believe he will be pleased by the results of his treatments here. Much to even my surprise, when he removed the mask an hour later and I asked how he felt, he said in a perfectly clear voice 'I feel quite fine'. Before the pressure was completely released, Susan was talking to him through the telephone system, with tears in her eyes. He regressed very slightly that evening but has come back entirely after eight treatments. Early intervention is tantamount for best results. We saw my father make a complete recovery, now our web developer (age 45) and our very special client from Maine (age 52) who 4 years post stroke can now hug his wife with both arms, walk along a rocky path at his cottage and he just went fishing with his buddies for the first time in years. Although he muses that, he caught nothing!

Sincerely, Don Dalgleish


Q: How does HBO2 work to help reduce cerebral vascular accident ischemia?

Answer: In acute and semi-acute neurologic conditions, where there is no matrix, pressurized oxygen has beneficial effects in that it not only dissolves in cerebrospinal fluid, but also:

  1. Reduces cerebral edema;
  2. Reduces intracranial pressure;
  3. Elevates diffusional driving force for oxygen, increasing tissue oxygen availability;
  4. Restores the integrity of the blood-brain barrier and cell membranes;
  5. Neutralizes toxic amines;
  6. Increases neovascularization (over time);
  7. Acts as a scavenger of free radicals;
  8. Promotes phagocytosis (thereby internal debridement);
  9. Stimulates angiogenesis (over time);
  10. Reactivates idling neurons;
  11. Inhibits anaerobic glycolysis;
  12. Promotes epithelization;
  13. Deglutination of platelets;
  14. Makes available molecular oxygen for immediate use without energy transfer;
  15. Reduces lactate peak in hypoxia;


Congress on Cerebral Ischemia, Vascular Demential, Epilepsy and CNS Injury. New Aspects of Prevention and Treatment from Space and Underwater Explorations. World Federation of Neurology May9-13, 1998 Washington, D.C., US. Prepared by Drs. George and Virginia Howard - Statisticians.

  1. Astrup, Siesjo BK, Symon L. Thresholds of ischemia; the ischemic penumbra. Stroke 1981; 12: 723725.
  2. Dai J. Swaab DF, Buijs RAM. Recovery of axonal transport in "dead neurons" Lancet 1998; 351: 500.
  3. Editorial. Treatment for stroke?. Lancet 1991; 337: 1129-1131.
  4. Nighoghossian N. Trouillas P. Adeleine P. Salford F. Hyperbaric oxygen in the treatment of the acute ischemic stroke. A double-blind pilot study. Stroke 1995; 26(8): 1369-1372.
  5. Heyman A., et al. The use of hyperbaric oxygenation in the treatment of cerebral ischemia and infarction. Circulation, Supplement 2: May, 1966; (33-34): 20-27.
  6. Anderson D, et al. A pilot study of hyperbaric oxygen in the treatment of human stroke. Stroke 1991; 22: 1137-1142.
  7. Kazantseva NV, Makarova LD, Kabanov M, et al. Clinical effects of mechanisms of action of higher pressure in treatment of stroke. European J. Neurology June 1, 1997; 4, Suppl 1: 190.
  8. Neubauer RA, End E. Hyperbaric oxygenation as an adjunct therapy in strokes due to thrombosis. A review of 122 patients. Stroke 1980; 11 (3): 297-300.

In 1908, R. Pfeifer reported autopsy studies of human brains that had undergone exploratory punctures, months before their deaths. He recognized on the margins of the resulting brain injuries that the scars had numerous nerves and nerve fibres that were regenerating. That these "marginal" neurons remain intact, alive and in place for more than the few months reported by Pfeifer was reported in 1934. Cyril B. Courville demonstrated the persistence of the processes of disintegration, of phagocytosis and repair in the brain of a 57 year old who had been shot in the head twenty-two years previously. Seriously damaged nerve cells had maintained their morphologic identity throughout this long period.

In summarizing this case Courville stated, " Morphologically, crippled nerve cells may persist in the margins of wounds of the brain for many years." "Even after a prolonged interval the larger nerve fibers continue to show regressive change at the margins of wounds of the brain." The concept of an ischemic marginal zone surrounding a central core of infarcted brain tissue as a component of stroke induced damage was further developed by Astrup, Symon, Branston, and Lassen in 1977. Their baboon studies showed that electrical activity was lost at the periphery of a cerebral infarct when the blood flow fell below 15 ml/100g/min while neuronal death began to occur when blood flow fell to 6-8 ml/100 g/min.

These low blood flow values may be used to define an area surrounding an infarct where the tissues remain alive but are not functioning called the "ischemic penumbra". Dorland’s Illustrated Medical Dictionary (28th ed., 1994) defines the ischemic penumbra as "an area of moderately ischemic brain tissue surrounding an area of more severe ischemia; blood flow to this area may be enhanced in order to prevent the spread of a cerebral infarction." Results have accumulated supporting the concept of the ischemic penumbra as a dynamic process of impaired perfusion and metabolism eventually propagating with time from the center of ischemia to the neighboring tissue.

As mediators and modulators of this process, waves of depolarization, extra cellular increases in excitatory amino acids, activation of Ca++ channels, intracellular calcium deposition, induction of immediate early genes and expression of heat-shock proteins all play a role. (Heiss, WD, Graf, R 1994) Spontaneous electrical activity is impaired when cerebral blood flow is reduced to about 60% of control. (Hossmann, KA et al 1980) (Moraweth RB et al 1979) Protein synthesis is suppressed 50% at a cerebral blood flow of 40% even before spontaneous electrical activity is impaired. (Mies, G. et al. 1991). Branston (et al 1974) demonstrated deterioration in the amplitude of somatically evoked potentials at approximately 34% of control blood flow, which is also the level of blood flow at which glucose begins to be utilized more rapidly due to oxygen-debt inhibition of mitochondrial metabolism and oxidative phosphorylation.

Thus, glycolysis is stimulated in order to maintain ATP levels. This produces lactic acid, which accumulates because flow is reduced. Since ATP production by glycolysis cannot fully compensate for oxidative phosphorylation, AMP and purine levels increase and tissue adenylates are irreversibly lost either enzymatically or through blood clearance. Reduction in cerebral blood flow below 30 ml/100 g/min suppresses the adenylate cyclase and protein kinase C system (Tanaka K et al. 1993).

The loss of adenylates, accumulation of lactic acid with a lowering of the pH and the formation of free radicals with subsequent oxidation of blood vessels walls, blood components and brain tissues results in induction of early response genes, expression of heat-shock proteins and diminished blood vessel wall and brain tissue protein synthesis and responsiveness (Paschen, W. et al 1992) Other studies have implicated a multifactorial interaction at the ischemic blood-endothelial interface of Factor VIII/von Willebrand factor, prostanoids, leukocytes, platelets, platelet-activating factor, leukotrienes, adhesion receptors, monocytes/macrophages, fibrinogen, viscosity and cytokines that can impair microvascular perfusion (Hallenbeck JM 1994) Disruption of the blood brain barrier occurs in focal cerebral ischemia (the animal model of stroke) and the degree of the disruption correlates inversely with cerebral blood flow. (Yang GY & Betz, AL 1994) Free oxygen radicals have been shown to disrupt the blood brain barrier in focal ischemia, which allows large molecules to pass through into the brain. Free radicals inhibit rather than cause post ischemic hyperemia.(Tasdemiroglu E. et al 1994), which is one more mechanism that causes stagnation of blood flow through the ischemic penumbral zone.

When blood flow is further reduced to approximately 15%, synaptic transmission is abolished (Branston, NM et al. 1977) (Heiss, WD et al 1976), extra cellular potassium increases and ATP falls proportionately. A massive release of extra cellular potassium occurs at blood flow levels below 10%, ATP is totally exhausted, neurons depolarize, cellular ion homeostasis breaks down, and cell death occurs. (Astrup,et al. 1977. (Welsh, F.A. et al. 1978) (Paschen, W et al 1992) The margins of an infarct are usually strikingly irregular. The explanation for this probably lies in the preservation of the circulation in some limited areas through better anastomosis of collateral vessels. (W. Freeman 1933) (Tamura A. et al. 1981), (Tyson GW) The debate about the size of the penumbra revolves around the methods used to study it. The morphological evidence is much less than the size shown by autoradiography (rat-Tyson et al 1984; cat-Ginsberg et al, 1976) and this area is much less than that shown by functional assessment (Symon et al.1976). Substantial areas of flow reduction beyond the infarcted area(s) can be delineated by CT and MRI, while concurrently; oxygen utilization is decreased in these areas (Raynaud et al., 1987)(Benveniste H et al 1991).

Repeat multitracer PET studies with human stroke victims have shown viable tissue in the border zone of ischemia up to 48 hours after the cerebrovascular attack. With few exceptions, these tissues suffer progressive metabolic derangement and had decreased cerebral metabolic rates of oxygen (-17.2% vs -26.1% as compared to normal mirror image regions of interests) within two weeks after the stroke. (WD Heiss et al. 1992). For many years, cerebral ischemia has been thought to release glutamate from the hypoxic, damaged cells and this glutamate was thought to potentate and propagate the initial hypoxic damage. Recently described, an alternative explanation for glutamate-mediated injury is hypoxia as well but caused by peri-infarct spreading depression-like depolarizations.

These irregular depolarizations are thought to initiate or worsen hypoxic episodes (due to energy expenditures) and cause a further suppression in protein synthesis, a gradual deterioration in energy metabolism, and a progression of irreversibly damaged tissue into the penumbra zone. Thus, "interventions to improve ischemic resistance should therefore aim at improving the oxygen supply or reducing the metabolic workload in the penumbra region." (Hossmann KA 1994) Focal cerebral ischemia is the animal model of stroke and in this model; there is evidence for a reduction of the number of perfused capillaries in the affected penumbral areas.

This loss of capillary perfusion is probably the result of a combination of changes that occur in the terminal capillary bed in the wake of the acute ischemic process. RBC aggregation, platelet aggregation, endothelial swelling, increased blood and plasma viscosity, etc are just some of the factors that contribute to the loss or decrease in the flow properties of red cells through ischemic tissue capillaries. Plasma, on the other hand, has been shown to reach all ischemic and post-ischemic capillaries and is able to pass through capillaries where red cells are no longer able to pass due to the constrictive and restrictive changes created by the ischemic process. (K.Kogure, K.A. Hossmann and B.K.Siesjo 1993) One of the mechanisms of action of hyperbaric oxygen is to increase the oxygen solubility in blood plasma. It is possible to dissolve sufficient oxygen (. i.e. 6 vol% in plasma) to meet the oxygen needs of the brain. (K.K.Jain, 1996) Thus in the acute stroke patient, the use of hyperbaric oxygen is able to provide oxygen to ischemic neurons and to keep them alive while either endogenous or exogenous fibrinolytic mechanisms are brought to bear on the cerebral thrombosis that is causing the ischemia. This results in the salvage of the ischemic penumbra to a degree impossible with any other therapy.

Summary of the effects of HBO2 both in acute and semi-acute and long-term neurologic conditions: HBO2 reduces any pressure within the brain caused by swelling, restoring the functions of the blood brain barrier and cell membrane; It neutralizes toxic products in the brain, and over a period of time, enhances growth of new blood vessels; It also acts as a scavenger of free radicals and promotes internal cleaning of debris; HBO2 also reduces the stickiness of blood products (white blood cells and platelets), and makes oxygen available for use without energy transfer (when the hemoglobin carries oxygen, it requires energy to deliver to the tissue spaces); With HBO2 the free oxygen is available immediately for metabolic use.



Why is there such a lack of knowledge among doctors about HBOT?


There are several reasons. One is that many doctors do not realize that HBOT can force oxygen into the body’s tissues. Most Diseases affect an area’s microcirculation, the circulation through the tiny capillaries that connect arteries to the veins.

Reference: “Hyperbaric Oxygen Therapy,” Dr Richard Neubauer M.D.


How is the use of HBOT different from oxygen in normal atmosphere?


The normal use of oxygen forces oxygen into the red blood cells only, which usually carry oxygen. However, the administration of high- pressure oxygen forces oxygen into the blood plasma, the liquid part of the blood, which normally doesn’t carry the life giving gas. (oxygen)


What is the effect of high-pressure oxygen in the plasma?


By forcing oxygen into the blood plasma, and not just the red blood cells, HBOT can help bring oxygen to the areas of the body which circulation has been impaired.


Where does the dissolved oxygen in the plasma go from there?


Under Hyperbaric Oxygen Conditions oxygen not only dissolves in plasma, but in all the body’s fluids, such as the lymph and the fluid surrounding the bran and spine, as well as in the bone morrow.


How many published studies are there on HBOT?


Over 30,000 scientific studies on HBOT published in medical journals, diving medicine, and clinical journals.



How does using HBOT help relieve brain swelling?


Hyperbaric Oxygen can help reduce brain swelling in different disorders, Stroke, T.B.I., and other disorders where swelling, edema, and inflammation is a problem. Drugs can reduce this swelling, however there is the need to supply the brain with needed oxygen. HBOT is helpful in reducing brain swelling by causing the vessels to contract. Once the extra fluid around the brain cells is drained away, the cells can function more effectively. It allows cell wastes to be more easily removed, which keeps the wastes from building up.


Can Hyperbaric Oxygen help reduce the spasticity in some patients?


With different disorders as in stroke, C.P., T.B.I., Closed head injury, and others, sometimes the patient’s muscles often become spastic or rigid. This spasticity becomes the greatest obstacle to physical therapy. HBOT has been known to be an effective and nontoxic anti-spasticity measure. Along with Physical Therapies, HBOT helps reduces spasticity. It is not exactly clear how HBOT reduces Spasticity, but Medical Physicians who are involved with HBOT believe that it has to do with activation of the neurons in the penumbra zone of the brain.


How does Hyperbaric Oxygen Therapy work well with Physical Therapies, such as P.T. and O.T.?


HBOT works very well with many Physical Therapies. In exercise and other forms of movement. Physical Therapy reorganizes the neurons awakened by HBOT. It can be used along side various types of rehabilitative therapies, as speech, occupational therapy, and biofeedback. Hyperbaric Oxygen Therapy is a part of the overall comprehensive plan.


How can HBOT help dormant brain cells with oxygen?


Just giving oxygen at the surface or at normal atmosphere sometimes is not enough to improve oxygen deficiency. Normal pressure simply cannot put enough oxygen into the blood stream or the cerebrospinal fluid. HBOT with pressure greater than the normal atmosphere helps improve oxygen deficiency in some patients. It is hoped that in the future, Hyperbaric Oxygen may be used in emergency trauma centers to reduce edema and brain swelling.


There is strong evidence that Hyperbaric Oxygen Therapy can help by preventing burn shock, or circulatory failure produced by massive fluid loss. Hyperbaric Oxygen Therapy inhibits wound infection, both by helping to support the body’s infection- fighting white cells and by helping to increase the effectiveness of antibiotics.

Hyperbaric Oxygen Therapy aids in the survival of skin grafts and flaps by reducing the rate of complications and reducing the need for fluids.

Often HBOT help the patient cope with other serious problems that accompany burns, such as smoke inhalation and carbon monoxide poisoning.

All of these factors help to speed healing and increase the survival rate of the patients.

In 1974, a study by Dr. G.B. Hart and colleagues looked at 191 human burn patients. The results showed decreases in healing time, complication rate, and mortality rate for the patients who were treated with HBOT within the first 24 hours after the injury. The researchers concluded that while HBOT was not a cure for all for burn patients, it could play a significant role in a total burn treatment program.

Other parts of a burn treatment programs include:

  • Wound cleaning.
  • Debridement or removal of the dead skin.
  • Use of intravenous fluids to counteract the fluid loss.
  • Treatment of lung disorders caused by smoke inhalation and exposure to toxic gases.
  • Antibiotics and tetanus booster.
  • The use of splints and pressure garments, which can help, preserve appearance and function.

It is hoped that in the future, Hyperbaric Oxygen will be a part of the treatment for burns and in every burn center.


How can the use of Hyperbaric Oxygen Therapy help in the case of bone healing or infections?


HBOT can help to heal bone disorders by stimulating both the osteoclasts and the osteoblasts. This helps and leads to the re-absorption of dead bone and the creation of new bone. In addition, HBOT stimulates the production of new blood vessels, so that the growing bone receives a steady supply of nutrients, including oxygen. This blood vessel network does two other things: it helps support the function of the osteoclasts, and brings infection fighting white blood cells to the area.

Osteomyelitis is a bacterial infection that usually involves both the outer layers of the bone and the inner bone marrow. Staphylococci, is a common form of bacteria that can cause infections ranging from pimples to meningitis.

  • Chronic osteomyelitis may follow an acute form or may develop over time; this is also when the acute form is not completely cured by treatment.
  • Long –term Osteomyelitis which in some cases continues for years.
  • Refractory osteomyelitis is a term referring to the condition of bone infection that did not respond to either surgical or antibiotic therapy

Part of the difficultly in treating osteomyelitis lies in the fact that it causes a lack of oxygen in the tissues. HBOT, by providing forced oxygenation, helps fight this disorder along with antibiotic therapy and or surgical intervention. Hyperbaric Oxygen Therapy helps preserve healthy bone, restore, and help build new bone and helps with the immune system. In some cases, in both bones and wounds, HBOT draws a clear line by which the surgeon can aid in the removal of dead or diseased bones. These types of infections can occur sometimes in the extraction of a tooth.

A good three-part treatment for bone infections includes the use of antibiotics, surgery to remove the dead bone, and HBOT as a supporting or adjunct treatment. There are some surgeons who are using HBOT before and after surgery.

Please refer to references at the end of this section.


Fractures and HBOT


Would anyone treat a 73-year-old man who had a fall and as a result had Fractures?

How may HBOT help fractures to heal?


Yes and some reasons are:

  1. Edema, because of the poor solubility of oxygen in water limits oxygen transport. Oxygen under hyperbaric conditions, by reduces blood flow also reduces tissue hydrostatic pressure allowing better lymphatic drainage.
  2. Fracture, because when a bone is broken the blood supply is damaged and oxygen transport is reduced. Healing is oxygen dependent In addition; the rate of bone formation, even in uncomplicated fractures is improved by intermittent high dosage oxygen.
  3. Soft tissue damage. The rate of collagen formation and the tensile strength is doubled under hyperoxic conditions.
  4. The cerebral effects may be due to fat embolism, which responds well to hyperbaric oxygen therapy.

Philip James M.D.
Wolfson Hyperbaric Medicine Unit
Ninewells Medical School

Reprinted with Permission


What are the Beneficial Mechanisms?

Several beneficial mechanisms are associated with intermittent exposure to hyperbaric doses of oxygen. Either alone, or more commonly in combination with other medical and surgical procedures, these mechanisms serve to enhance the healing process of treatable conditions.

1. HYPEROXYGENATION: provides immediate support to poorly perfused tissue in areas of compromised blood flow. The elevated pressure within the hyperbaric chamber results in a 10-15 fold increase in plasma oxygen concentration. This translates to arterial oxygen values of between 1,500 and 2000 mmHg, thereby producing a four-fold increase in the diffusing distance of oxygen from functioning capillaries. While this form of hyper-oxygenation is only a temporary measure, it will often serve to buy time and maintain tissue viability until corrective measures can be implemented or a new blood supply established.

2. NEOVASCULARIZATION: represents an indirect and delayed response to hyperbaric oxygen exposure. Therapeutic effects include enhanced fibroblast division, neo-formation of collagen, and capillary angiogenesis in areas of sluggish neovascularization such as late radiation damaged tissue, refractory osteomyelitis, and chronic ulcerations in soft tissue.

3. HYPEROXIA: enhanced ANTIMICROBIAL ACTIVITY has been demonstrated at a number of levels. Hyperbaric oxygen causes toxin inhibition and toxin inactivation in Clostridial perfringens infections (gas gangrene). Hyperoxia enhances phagocytosis and white cell oxidative killing, and has been shown to enhance amino glycoside activity. Recent research has demonstrated a prolonged post-antibiotic effect, when hyperbaric oxygen is combined with tobramycin against Pseudomonas aeroginosa.

4. DIRECT PRESSURE: utilizes the concept of Boyle's Law to reduce the volume of intravascular or other free gas. For more than a century, this mechanism has formed the basis for hyperbaric oxygen therapy as the standard of care for decompression sickness and cerebral arterial gas embolism. Commonly associated with divers, CAGE is a frequent introgenicevent in modern medical practice. It results in significant morbidity and mortality and remains grossly under diagnosed.

5. Hyperoxia-induced VASOCONSTRICTION is another important mechanism. It occurs without component hypoxia, and is helpful in managing intermediate compartment syndrome and other acute ischemias in injured extremities, and reducing interstitial edema in grafted tissue. Studies in burn wound applications have indicated a significant decrease in fluid resuscitation requirements when hyperbaric oxygen therapy is added to standard burn wound management protocols.

6. ATTENUATION OF REPERFUSION INJURY: is the most recent mechanism to be discovered. Much of the damage associated with reperfusion is brought about by the inappropriate activation of leukocytes. Following an ischemic interval, the total injury pattern is the result of two components: a direct irreversible injury component from hypoxia, and an indirect injury, which is largely mediated by the inappropriate activation of leukocytes. Hyperbaric oxygen reduces the indirect component of injury by preventing such activation. The net effect is the preservation of marginal tissues that may otherwise be lost to ischemia- re-perfusion injury.



When do you usually see a change?


Every patient is different, every disorder is different. However, when we speak with patients, for example a child with Cerebral Palsy, I often will allow for a visual picture, which the parents can use to help understand HBOT, duration and improvements.

Hyperbaric Oxygen will reduce inflammation and edema and restore circulation. If needed it will re- grow new blood vessels, fire up idling neurons and “re-route” information within the brain. We use the time of 40 treatments as a guideline, because studies and data show that this is about what it takes for a wound. Nevertheless, all patients are different. Patients need to realize that we are actually growing new connective tissue when under hyperbaric conditions and that new tiny blood vessels or capillaries are grown. This takes an enormous amount of energy by the body and good nutrition is needed with hyperbaric oxygen therapy. For example, if you have a field that is void of vegetation and you water the field, you may get sparse green growth, however, if you build an irrigation system and permanently water the field, you will have started a system that will be able to produce vegetation all year long. Hence, Hyperbaric Oxygen Therapy is the building block by which the brain now begins to learn, and gain motor skills. This is usually done by the first set or sessions of HBOT.


How many sessions will this take?


One must realize that every person is different, no two are alike, and no brain disorders are alike. Therefore, it is important to build collateral circulation. On a very general rule, most patients will have one or two sessions of 40 each and some require boosters or maintenance.


Regarding Cerebral Palsy and other brain disorders, what is the time frame in between sessions?


Dr Paul Harch M.D. recommends about a month to six weeks. The break between sessions may vary slightly however, the break itself is very important.

“The most significant improvements are usually seen after the sessions are over.”

Reference: (Harch, Hughes)


Why is that, “The most significant improvements are usually seen after the sessions are over.”?


We must not think of Hyperbaric Oxygen Therapy as forty sessions, rather just 40 hours of therapy. Sometimes, the improvement is seen later after the treatment is over. This is because after the brain is re-vasculated and new blood flow begins in the area that is otherwise low in blood flow, it takes time for the brain one again uses this injured portion of the brain. Just as an implanted organ or a skin graft takes time to become useful. One must note, that with young children, HBOT is a building block to normalize functions and allow the child to learn. For example: If brain blood flow is restored in a child who has never stood or walked, we now have the building block to allow Physical Therapies to work with the child and normalize them by means of on going Physical Therapy.


Should our child or the patient have physical Therapy along with HBOT?


Hyperbaric Oxygen is the building block by which the patient will be better equipped to learn and maintain Physical Therapy. HBOT goes hand and hand with your ongoing PT, OT and alternative therapies. If possible, continue with your own going therapy during HBOT sessions. See prior question.


Can seizures can be beneficial?


I am not aware of any evidence that seizures improve patients but it IS a sign of activity and therefore they may be a sign of recovery. Note that seizures may result from the withdrawal of drugs e.g. baclofen Ref Barker I, Grant IS. Convulsions after abrupt withdrawal of baclofen. Lancet 1982;ii:556-7.

He also asked if when I recommended in my post that oxygen should be given post seizure if I meant be under hyperbaric conditions. Oxygen given immediately at high flow (i.e. as close to 100% as possible) at normal atmospheric pressure ( atm abs) will probably be enough to relieve the hypoxia post seizure. The key is immediate administration as lactic acid appears quickly.

Ref Miller SP, Weiss J, Barnwell A, et al. Seizure-associated brain injury in term newborns with perinatal asphyxia. Neurology 2002;58:542-8.

Seizures and hypoxia open the blood-brain barrier and this will if unchecked lead to edema and inevitably oxygen transport limitation.

Best wishes to all

Philip James MD