Slark Hyperbaric Unit

Hyperbaric Oxygen Therapy (HBOT)

Hyperbaric oxygen therapy has proven to be of value in the treatment of various conditions from decompression illness and carbon monoxide exposure to the treatment of chronic non-healing wounds and radiation damage.

Hyperbaric oxygen therapy is the administration of 100% oxygen at pressures greater than normal atmospheric (sea level) pressure. However, to be effective, the pressure must be greater than 2 atmospheres.
You will be treated at the appropriate pressure that has proven to be the most effective in the treatment of your condition.

Oxygen Administration

Hyperbaric oxygen therapy is provided by first pressurising the recompression chamber with air. You then breathe oxygen through a snugly fitting mask or an oxygen hood. This is the “treatment”.

During this treatment period you may sit in a chair or lie on a bunk and read a magazine or just listen to the radio. The length of each treatment will vary depending on the dose of oxygen prescribed but the treatment period is punctuated with regular 5-minute breaks from the oxygen mask or hood. The timing of these breaks is quite crucial and you will be advised when you may take a break.

Assistance

There will always be an attendant in the recompression chamber with you, who has been trained to monitor your progress and well-being. The chamber attendant will also carry out the occasional minor technical task to ensure your safety and comfort. The chamber can accommodate 5 patients so there will usually be others for company.

Chamber Operation

The diving supervisor, who is always available outside the chamber, is responsible for maintaining your safety and comfort and for keeping an accurate record of pressure and timing for the treatment. Pressurisation of the chamber is a noisy process. Ear defenders can be worn during pressurisation and during any periods of ‘flushing’ the chamber atmosphere. The chamber atmosphere is continuously monitored at the control panel and the attendant regularly gives ‘weather’ reports.

Procedure

You will be asked to remove your outdoor clothing, put on one of the “scrub” tops and bottoms which are made from cotton fabric. Please chat to staff if you think this will be a problem.  Occupants entering the chamber remove their shoes and ensure they are not carrying any “prohibited” goods such as oil or grease that may be on shoe soles. The door is shut and everyone may don ear defenders if required. Pressurisation begins and you start to “equalise your ears”. Once the required pressure is reached assistance is given to put on your oxygen mask or hood. Then you breathe normally. The attendant will instruct you what to do and when.

Possible Complications

Because the chamber is a relatively confined space in which oxygen is being administered, all possible measures are taken to minimise the risk of fire. All flammable materials are “prohibited” from the chamber and reading material is limited to one book each.

Clothing is restricted to the issued scrubs, t shirts and tops or sweatshirts worn over your own underwear. No cigarettes, matches, lighters, electronic gadgets including cellular phones, alcohol or oil based fluids are permitted. Pens are also restricted from entry into the chamber but pencils are fine. Most normal wristwatches are not made to withstand changes in pressure so unless yours is a diving watch you are advised not to wear it during a treatment.

If you have questions about any item please do not hesitate to ask the attendant or the diving supervisor.

The effect of pressure changes on your middle ears requires you to actively “clear your ears”. You will be coached to do this and you should begin “clearing your ears” from the very start of pressurisation. If at any time you feel the slightest discomfort in your ears, please inform the attendant immediately and help will be given.

Some techniques to clear your ears include swallowing, yawning, clicking your jaw, turning your head, holding your nose and breathing out against a closed throat (valsalva), chewing gum or drinking water.

Breathing oxygen at high pressures may also cause a reaction similar to an epileptic fit in some susceptible people. This is a relatively rare occurrence. If you do suffer such a reaction you will suffer no after-effects from it. Prior to this reaction happening the person would feel ‘odd’, perhaps nauseated, may have some changes in vision or hearing or even feel twitches in their lips or face. If you ever feel anything out of the ordinary that concerns you please promptly inform the attendant.

Following Treatment

If you are being treated for decompression illness you are advised not to dive, fly or ascend to an altitude of 300 metres or more above sea level for one month following your initial injury. If you are being treated for any other medical condition these restrictions do not apply to you, although you should discuss any plans to fly on the same day as treatment with one of the medical staff.

Your Health

If you have a cold you may not be fit to 'dive' because you may not be able to clear your ears or your sinuses may not be able to “equalise” themselves. Please inform the staff at any time if you feel unwell. If you are to have a prolonged course of treatment and you wear glasses for reading you may find that your vision has improved. This is a temporary change and you are recommended not to change your glasses over the course of the treatment or for a short period afterwards.

If you have cataracts you are advised to have an ophthalmologist examine your eyes prior to diving as cataract progression may be affected by hyperbaric oxygen. From time to time, staff may repeat lung function or eye tests, which you may have had prior to commencing treatment, this is routine.

Please do not hesitate to ask the staff about any aspect of your treatment and progress.

When scuba diving, additional oxygen and nitrogen dissolve in body tissues. The additional oxygen is consumed by the tissues, but the excess nitrogen must diffuse out by the blood during decompression.

During or after ascent this excess nitrogen gas can form bubbles in the tissues, analogous to the carbon dioxide bubbles that form when a carbonated drink container is opened.

These bubbles may then cause symptoms that are referred to as decompression sickness (“DCS” or “the bends”). Trapping of gas within the lungs during ascent, either because the lung is diseased or because of breath-holding, can cause bubbles to be forced into the bloodstream (“arterial gas embolism” or “AGE”), where they can block the flow of blood or damage the lining of blood vessels supplying critical organs such as the brain. AGE can also occur in non-divers, due to entry of air into the body, such as during medical, diagnostic or therapeutic procedures.

Symptoms of DCS or AGE can include joint pain, numbness, tingling, skin rash, extreme fatigue, weakness of arms or legs, dizziness, loss of hearing, and in serious cases, complete paralysis or unconsciousness. Emergency treatment of DCS or AGE includes administration of oxygen and measures to maintain adequate blood pressure, such as lying the patient down and fluid (either oral or intravenous, depending upon availability and severity of the illness).

Definitive treatment for DCS or AGE is administration of 100% oxygen at increased atmospheric pressure in a hyperbaric chamber (typically at a pressure 2-3 times greater than normal atmospheric pressure). While some delay in transporting a patient to a hyperbaric chamber is usually unavoidable, the success in relieving symptoms is greater if the treatment is administered within a few hours after the onset of symptoms. Some improvement might be expected, particularly in mild cases, even after a day or more of delay. The vast majority of cases respond satisfactorily to a single hyperbaric oxygen treatment. Sometimes, repetitive treatments are recommended until no further improvement can be observed.

A small minority of divers with severe neurological injury may require 15-20 repetitive treatments. The success of hyperbaric oxygen treatment for DCS or AGE over many decades has proven its value and continues to be the standard of care for the treatment of these disorders.

References:

1. Francis TJR, Gorman DF. Pathogenesis of the decompression disorders. In: Bennett PB, Elliott DH, eds. The Physiology and Medicine of Diving. Philadelphia: W.B. Saunders, 1993:454-480.
2. Elliott DH, Moon RE. Manifestations of the decompression disorders. In: Bennett PB, Elliott DH, eds. The Physiology and Medicine of Diving. Philadelphia, PA: WB Saunders, 1993:481-505.
3. Moon RE, Sheffield PJ. Guidelines for treatment of decompression illness. Aviat Space Environ Med 1997;68:234-243.
4. Navy Department. US Navy Diving Manual. Vol 1 Revision 3: Air Diving. NAVSEA 0994-LP-001-9110. Flagstaff, AZ: Best, 1993.
5. Ball R. Effect of severity, time to recompression with oxygen, and retreatment on outcome in forty-nine cases of spinal cord decompression sickness. Undersea Hyperbaric Med 1993;20:133-145.
6. Kizer KW. Delayed treatment of dysbarism: a retrospective review of 50 cases. JAMA 1982; 247: 2555-8.
7. Moon RE, Gorman D: Treatment of the Decompression Disorders. In: The Physiology and Medicine of Diving. Edited by Bennett PB, Elliott DH. Philadelphia, PA, Saunders, 1993, pp 506-541.

Air or gas embolism occurs when gas bubbles enter arteries, veins and/or capillaries. This results in reduced blood flow and poor oxygen delivery to the areas supplied by the affected circulation. If not fatal, gas embolism can result in severe, long-standing and irreversible physical and emotional disabilities.

There can be weakness or paralysis in the limbs; vision can be impaired or absent; brain, heart, lung and other organ damage may occur. Limited use of remaining functions can be sufficiently severe that total disability results. Those who do not die may be limited to walking with canes, crutches or walkers. Those more severely disabled may be wheelchair confined or bedridden. These outcomes may be permanent and may severely impact quality of life.

Maximal medical treatment of the condition is necessary to ensure the best possible degree of recovery from this potentially disastrous problem. Hyperbaric oxygen has been shown to reduce the size of bubbles obstructing circulation. The increased pressure in the hyperbaric chamber reduces bubble size and drives the remaining gas into physical solution, while the high oxygen pressure washes out inert gas from the bubble. When bubbles are smaller or resolved, blood flow resumes. Poorly oxygenated tissues then receive higher levels of oxygen delivery.

Another problem in gas embolism is that vessels obstructed by bubbles may leak fluid into surrounding tissues, resulting in swelling. Such swelling can further reduce tissue blood flow. When flow is restored, the local swelling will subside with resultant improvement in circulation and oxygen supply. Finally, the high levels of oxygen provided in the hyperbaric chamber have the potential to immediately restore cellular oxygen levels while blood flow impairment and tissue swelling are being corrected.  Hyperbaric oxygen treatment is the primary treatment for gas embolism and a major review of reported cases clearly indicates superior outcomes with its use compared to non-recompression treatment.

References:

1. Mushkat Y, Luxman D, Nachum Z, David MP, Melamed Y. Gas embolism complicating obstetric or gynecologic procedures. Case reports and review of the literature. European Journal of Obstetrics, Gynecology, & Reproductive Biology 1995;63:97-103.
2. Boussuges A, Blanc P, Molenat F, Bergmann E, Sainty JM. Prognosis in iatrogenic gas embolism. Minerva Medica 1995;86:453-457.
3. Weiss LD, Van Meter KW. The applications of hyperbaric oxygen therapy in emergency medicine. American Journal of Emergency Medicine 1992;10:558-568.
4. Kindwall EP. Uses of hyperbaric oxygen therapy in the 1990s. Cleveland Clinic Journal of Medicine. 1992;59:517-528.
5. Dutka AJ. Air or gas embolism. In: Hyperbaric Oxygen Therapy: A Critical Review. Camporesi EM, Barker AC, eds. Bethesda, MD, Undersea and Hyperbaric Medical Society, 1991:1-10.

Carbon monoxide (CO) is a colourless, odourless gas produced as a by-product of combustion. Poisoning occurs by inhalation, either accidentally or intentionally (suicide attempt). CO poisoning is responsible for an estimated 40,000 emergency department visits and 1,000 accidental deaths in the United States annually.

Approximately 5-6% of patients evaluated in emergency departments for CO poisoning are treated with hyperbaric oxygen (HBO2). CO binds to haemoglobin in red blood cells at the sites usually utilized to carry oxygen to tissues. Oxygen, and especially hyperbaric oxygen, accelerates the clearance of CO from the body, thereby restoring oxygen delivery to sensitive tissues such as brain and heart. This has traditionally been considered to be the mechanism of benefit of HBO2. However, research published in the past few years has demonstrated a number of other mechanisms of toxicity from CO.

Blood vessel (vascular) injury from CO has been demonstrated to result from CO-induced production of nitric oxide-derived oxidants and cellular injury from activated white blood cells (neutrophils). CO also causes direct central nervous system cellular injury through mechanisms that include disturbance of energy metabolism and intracellular production of oxygen free radicals. In animal experiments, hyperbaric oxygen, but not normobaric oxygen (NBO2), has been demonstrated to block each of these mechanisms of toxicity.

Until ten years ago, the benefit of hyperbaric oxygen treatment of CO poisoning was demonstrated by comparing the clinical experience at institutions where HBO2 was used with that at facilities where it was not available. Since 1989, six randomized prospective trials have been reported comparing HBO2 with NBO2 treatment of acute CO poisoning. Of these, three demonstrate improved patient outcomes with hyperbaric oxygen, two report no difference between the two therapies, and one remains blinded with regard to the treatment administered. A full listing of the investigations, as well as a discussion of the study designs and findings, can be found in the UHMS Hyperbaric Oxygen Therapy Committee Report (available for purchase through this web site). The UHMS currently recommends HBO2 treatment of individuals with serious CO poisoning, as manifest by transient or prolonged unconsciousness, abnormal neurologic signs, cardiovascular dysfunction, or severe acidosis.

References:

1. Thom SR, Fisher D, Xu YA, Garner S, Ischiropoulos H. Role of nitric oxide-derived oxidantsin vascular injury from carbon monoxide in the rat. Am J Physiol 1999;276:H984-992.
2. Brown SD, Piantadosi CA. Recovery of energy metabolism in rat brain after carbon monoxide hypoxia. J Clin Invest 1991;89:666-672.
3. Hyperbaric Oxygen Therapy Committee. Hyperbaric Oxygen Therapy: 1999 Committee Report. Hampson NB, ed. Kensington, MD: Undersea and Hyperbaric Medical Society; 1999.
4. Hampson N, Dunford RG, Kramer CC, Norkool DM. Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. J Emerg Med 1995;13:227-231.

Clostridial myositis and myonecrosis is an acute, rapidly progressive infection of the soft tissues commonly known as “gas gangrene.” The infection is caused by one of several bacteria in the group known as “clostridium.” While over 150 species of clostridium have been identified, only a few commonly cause gas gangrene.

The infection typically spreads from a discrete focus of clostridium within the body. The original source can actually be within the body, as clostridium normally live in the gastrointestinal tract. Alternatively, the infection can originate outside the body, such as when infection results from contamination of wounds during trauma (e.g. motor vehicle accidents). Gas gangrene infection is severe and can advance quickly. Besides replicating and migrating, the organisms which cause gas gangrene produce poisons known as exotoxins. Exotoxins are capable of liquefying adjacent tissue and inhibiting local defence mechanisms which might normally contain a less virulent infection. As such, the advancing infection of gas gangrene may simply destroy healthy tissue in its path and spread over the course of hours.

Clostridium bacteria are “anaerobic,” meaning that they prefer low oxygen concentrations to grow. If clostridia are exposed to high amounts of oxygen, their replication, migration, and exotoxin production can be inhibited. This is the rationale for the use of hyperbaric oxygen in the treatment of gas gangrene.

Repeated treatment in the hyperbaric chamber has the potential to slow the progress of the infection while the two primary therapies, antibiotics and surgical resection of infected tissue, control it. The advantages of hyperbaric oxygen treatment in gas gangrene are two-fold. First, it may be lifesaving because exotoxin production is rapidly halted and less heroic surgery may be needed in gravely ill patients. Second, it may be limb and tissue-saving, possibly preventing limb amputation that might otherwise be necessary.

References

1. Bakker DJ. Clostridial myonecrosis. In Davis JC, Hunt TK, eds. Problem Wounds: The Role of Oxygen. New York: Elsevier, 1988:153-172.
2. Hirn M. Hyperbaric oxygen in the treatment of gas gangrene and perineal necrotizing fasciitis: A clinical and experimental study. Eur J Surg 1993;570 (Suppl):9-36.
3. Hyperbaric Oxygen Therapy Committee. Clostridial myositis and myonecrosis (gas gangrene). In: Hampson NB, ed. Hyperbaric Oxygen Therapy: 1999 Committee Report. Kensington, MD: Undersea and Hyperbaric Medical Society, 1999:13-16.
4. Stevens DL, Bryant AE, Adams K, Mader JT. Evaluation of therapy with hyperbaric oxygen for experimental infection with Clostridium perfringens. Clin Infect Dis 1993;17:231-237.

Crush injuries occur when body tissues are severely traumatized such as in motor vehicle accidents, falls, and gunshot wounds.

These injuries frequently occur in the extremities. When crush injuries are severe, the rate of complications such as infection, non-healing of fractures and amputations range up to 50%.

When used as an adjunct to orthopaedic surgery and antibiotics, hyperbaric oxygen (HBO2) therapy shows promise as a way to decrease complications from severe crush injuries. HBO2 increases oxygen delivery to the injured tissues, reduces swelling and provides an improved environment for healing and fighting infection.

Hyperbaric oxygen treatments should be started as soon after an injury as possible. They are usually continued for 5 to 6 days. A number of related conditions, including compartment syndromes, thermal burns, and threatened replantations are also benefited by hyperbaric oxygen, as discussed in other sections in this site.

References

1. Bouachour G, Cronier P, Gouello JP, Toulemonde JL, Talha A, Alquier P. Hyperbaric oxygen therapy in the management of crush injuries: A randomized double-blind placebo controlled clinical trial. J Trauma 1996;41:333-339.
2. Gustilo R. Management of Open Fractures and their Complications. W. B. Saunders, Philadelphia 1982;202-208.
3. Hyperbaric Oxygen Therapy Committee. Crush injuries, compartment syndromes, and other acute traumatic ischemias. In: Hyperbaric Oxygen Therapy: 1999 Committee Report. Hampson NB, ed. Undersea and Hyperbaric Medical Society, Kensington, MD 1999;17-21.
4. Strauss M. Crush injury, compartment syndrome and other acute traumatic peripheral ischemias. In: Hyperbaric Medicine Practice. Kindwall EP and Whelan HT, eds. Best Publishing, Flagstaff, AZ 1999; 753-778.

Problem wounds are those which fail to respond to established medical and surgical management. Such wounds usually develop in compromised hosts with multiple local and systemic factors contributing to inhibition of tissue repair. These include diabetic feet, compromised amputation sites, non healing traumatic wounds, and vascular insufficiency ulcers (ulcers with poor circulation).

All share the common problem of tissue hypoxia (low tissue oxygen level, usually related to impaired circulation). Diabetic foot wounds are one of the major complications of diabetes and an excellent example of the type of complicated wound which can be treated with hyperbaric oxygen. Fifty percent of all lower extremity amputations in the United States are due to diabetes, at a cost of more than one billion dollars per year. It is well known that many diabetics suffer circulatory disorders that create inadequate levels of oxygen to support wound healing.

Hyperbaric oxygen therapy is a treatment in which patients receive high concentrations of oxygen under pressure in order to increase the oxygen level in the blood and tissues. The elevation in tissue oxygen which occurs in the hyperbaric chamber induces significant changes in the wound repair process that promote healing. When hyperbaric treatment is used in conjunction with standard wound care, improved results have been demonstrated in the healing of difficult or limb threatening wounds as compared to routine wound care alone.

References

1. Cianci P. Adjunctive hyperbaric oxygen in the treatment of problem wounds: An economic analysis. In: Kindwall E, ed. Proceedings of the Eighth International Congress on Hyperbaric Medicine. San Pedro, CA: Best Publishing. 1984:213-216.
2. Cianci P, Petrone G, Drager S, Lueders H, Lee H, Shapiro R. Salvage of the problem wound and potential amputation with wound care and adjunctive hyperbaric oxygen therapy: An economic analysis. J Hyperbaric Med 1988;3:127-141.
3. Hunt TK. The physiology of wound healing. Ann Emerg Med 1988;17:1265-1273.
4. Stone JA, Cianci P. The adjunctive role of hyperbaric oxygen therapy in the treatment of lower extremity wounds in patients with diabetes. Diabetes Spectrum 1997;10:118-123.

For purpose of consideration of the use of hyperbaric oxygen (HBO2) therapy, exceptional blood loss anaemia is by definition loss of enough red blood cell mass to compromise sufficient oxygen delivery to tissue in patients who cannot be transfused for medical or religious reasons.

Medical reasons may include the threat of blood product incompatibility or concern for transmissible disease. Religious beliefs may prohibit the receipt of transfused blood products. Red blood cells (RBCs) contain the respiratory pigment haemoglobin (Hb). Haemoglobin has the powerful ability to pick up oxygen as RBCs pass through the blood vessels of the lungs. Haemoglobin then has the equally powerful ability to off-load oxygen in the tissues of the body’s organ systems.

If plasma were the only vehicle to deliver dissolved oxygen, each 100 ml of blood flowing to an organ system would carry only 0.3 ml of gaseous oxygen. The consumption of oxygen by human tissues far exceeds this. For instance, the kidney extracts approximately 2 ml of oxygen for every 100 ml of blood which circulates through it. From the same 100 ml of blood, the brain extracts approximately 6.5 ml and the heart 10.5 ml of oxygen. In most instances, humans average 15 grams of haemoglobin per 100 cc of blood. Each gram of haemoglobin transports 1.34 ml of oxygen. This is in addition to the oxygen carried by plasma. So, 100 ml of blood, by containing 15 grams of haemoglobin, can carry approximately 20 ml of gaseous oxygen (1.34 ml X 15 g Hb = 20 ml of oxygen).

In the 1960s, the Dutch thoracic surgeon Boerema demonstrated that one could exchange transfused piglets with a simulated plasma mixture of buffered normal saline (Ringer’s Lactate solution), dextrose and dextran. In this process, blood was removed from the blood vessels and the substitute liquid (without haemoglobin) replaced. He then pressurized the piglets in a hyperbaric chamber while the animals breathed 100% oxygen. By the trick of pressurization, enough oxygen could be dissolved in the simulated plasma mixture to supply tissue oxygen requirements. This was enough to adequately sustain the animal, as evidenced by the fact that the animals survived and could be brought out of the chamber to be successfully re-exchange transfused with their previously extracted blood.

As hyperbaric oxygen (or for that matter normobaric oxygen) administered for long periods can become toxic, intermittent administration of HBO2 is essential. This point has been demonstrated clinically by the American thoracic surgeon, George Hart. In 1974, he reported a series of 26 severe blood loss patients who were treated with HBO2 as an alternative to otherwise disallowed red blood cell transfusion. The survival rate was 70%.

Alternative approaches include use of fluorocarbons or stroma-free haemoglobin. While potentially promising, these treatment solutions still pose uncertainties for their potential ability to unfavourably alter the immune system. While erythropoietin may be used to stimulate the bone marrow to produce RBCs, HBO2 therapy only complements its use in exceptional blood-loss anaemia.

References:

1. Adir Y, Bitterman N, Katz E, Melamed Y, Bitterman H. Salutary consequences of oxygen therapy on the long-term outcome of hemorrhagic shock in awake, unrestrained rats. Undersea Hyperbaric Med 1993;22(1):23-30.
2. Boerema I, Meijne NG, Brummelkamp WH, Bouma S, Mensch MH, Kamermans F, Hanf S, Van Aalderen A. Life without blood. J Cardiovasc Surg 1960;182:133-146.
3. Castro O, Nesbit AE, Lyles D. Effect of a perfluorocarbon emulsion (Fluosol-DA) on reticuloendothelial system clearance function. Am J Hematol 1984;16:15-21.
4. Advanced Trauma Life Support for Doctors, Instruction Manuel, Chapter 3, Shock, American College of Surgeons, Chicago IL, 1997, pp 97-146.
5. Hart G. HBO and exceptional blood loss anemia. In: Hyperbaric Medicine Practice, Kindwall EP, Whalen HT, eds. Best Publishing Co, Flagstaff AZ, 1999; 741-751.
6. Hart GB, Lennon PA, Strauss MB. Hyperbaric oxygen in exceptional acute blood-loss anemia. J Hyperbaric Med 1987;2:205-210.
7. Hart GB. Exceptional blood loss anemia. Treatment with hyperbaric oxygen. JAMA 1974; 228: 1028-1029.

Abscess formation in the brain can be a devastating complication of sinus infections or bone infections (osteomyelitis) of the skull. Occasionally, abscesses are seeded from infection occurring in other parts of the body. Brain abscesses are frequently multiple.

One of the problems in treatment in treatment of brain abscesses relates to the fact that surgical drainage of their contents is often required for cure. Unfortunately, normal brain tissue surrounding the abscess may be unavoidably damaged by such surgery. Fine needle aspiration of the abscesses is being performed with greater frequency to avoid this problem.

Antibiotics may not penetrate well into brain abscesses. Furthermore, white blood cells, which kill infecting bacteria, may not have enough oxygen to effectively eliminate the infection when functioning deep in the abscess at a distance from their normal blood supply. It is well known that white blood cells require a minimum level of oxygen to kill bacteria. Most intracranial abscesses are caused by anaerobic bacteria (bacteria that function optimally in low oxygen concentrations).

Hyperbaric oxygen raises the environmental oxygen level in the region of the abscess, exposing the bacteria to levels which may inhibit or kill them, as well as providing sufficient oxygen for white blood cells to exercise their killing power.

The average mortality from intracranial abscess reported in six large series was 20%when hyperbaric oxygen (HBO2) was not used. Among the 48 known cases treated with HBO2 to date, the mortality has been only 2%. Additionally, most of the patients treated with hyperbaric oxygen have returned to their regular daily activity after recovery, with less apparent brain damage. Therapy with HBO2 carries minimal risk, so the risk-benefit ratio is not arguable.

References:

1. Lampl L, Frey G, Bock KH. Hyperbaric oxygen in intracranial abscesses - update of a series of 13 patients (abstract). Undersea Biomed Res 1992:19(Suppl):83.
2. Mathieu D, Wattel F, Neviere R, Bocquillon N. Intracranial infections and hyperbaric oxygen therapy: A five year experience (abstract). Undersea Hyperbaric Med 1999;26(Suppl):67.
3. Sutter B, Legat JA, Smolle-Juttner FM. Brain abscess before and after HBO. 12th Proc Sc Soc Physiol, Styria (Austria) 1996.

A number of types of infections of soft tissue may benefit from adjunct treatment with hyperbaric oxygen and are included in the category of “necrotizing soft tissue infections.” Names of such clinical syndromes include crepitant anaerobic cellulitis, progressive bacterial gangrene, necrotizing fasciitis, and nonclostridial myonecrosis. Gas gangrene (Clostridial myositis and myonecrosis) is a separate entity and is reviewed elsewhere in this site.

Necrotizing soft tissue infections may result from either a single strain or a mixed population of bacteria, typically occurring after trauma, surgery, and/or around foreign bodies. The individual affected by such infections is frequently compromised by conditions such as diabetes or vascular disease.

In addition to pre-existing host compromise, necrotizing soft tissue infections themselves may induce conditions adverse to control of the infection by normal host defence mechanisms. The infections commonly lower tissue oxygen levels, impairing the ability of the white blood cells (neutrophils) to fight infection. Toxins produced by bacteria involved may also inhibit neutrophil activity.

The primary treatments for necrotizing soft tissue infection are surgical excision of infected tissue and administration of appropriate antibiotics. In selected cases, addition of hyperbaric oxygen therapy may be both lifesaving and cost effective. Hyperbaric oxygen may be beneficial in several ways. Some of the bacteria involved in necrotizing soft tissue infections are “anaerobic,” growing most rapidly in a low oxygen environment. In the hyperbaric chamber, tissue oxygen levels may be raised sufficiently to inhibit bacterial growth. In addition, hyperbaric oxygen treatment may enhance the ability of neutrophils to kill bacteria, by a number of different mechanisms.

The use of hyperbaric oxygen for treatment of necrotizing soft tissue infections should be individualised. In specific instances where risk of morbidity and mortality are high, adjunct hyperbaric oxygen therapy should be considered.

References

1. Mader JT, Adams KR, Sutton TE. Infectious diseases: Pathophysiology and mechanisms of hyperbaric oxygen. J Hyperbaric Med 1987;2:133-140.
2. Knighton DR, Fiegel VD, Halverson T, Schneider S, Brown T, Wells CL. Oxygen as an antibiotic: The effect of inspired oxygen on bacterial clearance. Arch Surg 1990;125:97-100.
3. Brogan TV, Nizet V, Waldhausen JHT, Rubens CE, Clarke WR. Group A Streptococcal necrotizing fasciitis complicating primary varicella: A series of fourteen patients. Pediatr Infect Dis Jour 1995; 14:588-594.
4. Riseman JA, Zamboni WA, Curtis A, Graham DR, Konrad HR, Ross DS. Hyperbaric oxygen therapy for necrotizing fasciitis reduces mortality and the need for debridements. Surgery 1990;108-847-850.
5. Hollabaugh RS, Dmochowski RR, Hickerson WL Cox CE. Fournier’s Gangrene: Therapeutic impact of hyperbaric oxygen. Plast Reconstruct Surg 1998;101:94-100.

Osteomyelitis is an infection of the bone. Refractory osteomyelitis is a bone infection which has not responded to appropriate treatment. Hyperbaric oxygen increases the oxygen concentration in infected tissues, including bone.

Hyperbaric oxygen directly kills or inhibits the growth of organisms which prefer low oxygen concentrations (strict anaerobes). These effects occur through the oxygen induced production of toxic radicals or through an indirect effect medicated through the white blood cells (polymorphonuclear leukocytes).

Conversely, hyperbaric oxygen has no direct effect on organisms which prefer high oxygen concentrations (aerobes). In fact, hyperoxic conditions may induce aerobic organisms to produce increased concentrations enzymes protective against oxygen radicals (e.g. superoxide dismutase).

When hyperbaric oxygen increases the oxygen tension in infected tissue, however, the oxygen dependent killing mechanisms of the polymorphonuclear leukocyte are provided sufficient oxygen to function. Thus, hyperbaric oxygen treatment provides the necessary substrate (oxygen) for the killing of aerobic organisms by the polymorphonuclear leukocyte.

Hyperbaric oxygen also augments the efficacy of bacterial killing by certain antibiotics (aminoglycosides, vancomycin, quinolones and certain sulfonamides). Hyperbaric oxygen provides adequate oxygen for fibroblast activity, cells which promote healing in hypoxic tissues.

Finally hyperbaric oxygen prevents polymorphonuclear leukocytes from adhering to damaged blood vessel linings. This decreases the degree of inflammation which may accompany the surgical treatment of refractory osteomyelitis. Hyperbaric oxygen is used clinically for the treatment of refractory osteomyelitis as noted above. Hyperbaric oxygen is adjunctive therapy and is used with appropriate antibiotics, surgery and nutrition.

There are open, patients used as their own controls and randomized clinical studies supporting the use of HBO for the treatment of refractory osteomyelitis.

References:

1.Mader JT, Guckian JC, Glass DL, Reinarz JA. Therapy with hyperbaric oxygen for experimental osteomyelitis due to Staphylococcus aureus in rabbits. J Infect Dis 1978;138:312-318.
2. Mader JT, Brown GL, Guckian JC, Wells CH, Reinarz JA. A mechanism for the amelioration by hyperbaric oxygen of experimental staphylococcal osteomyelitis in rabbits. J Infect Dis 1980; 142:915-922.
3. Davis JC, Heckman JD, DeLee JC, Buckwold FJ. Chronic non-hematogenous osteomyelitis treated with adjuvant hyperbaric oxygen. J Bone Joint Surg 1986;68A:1210-1217.
4. Mader JT, Shirtliff ME, Calhoun JH. The Use of Hyperbaric Oxygen in the Treatment of Osteomyelitis. In: Hyperbaric Medicine Practice. Best Publishing Co. Flagstaff, Arizona.1999; 603-616.
5. Mader JT, Calhoun JH. Osteomyelitis. In: Principles and Practice of Infectious Diseases. GL Mandell, RG Douglas, JE Bennett Jr. (Eds). Churchill Livingstone, New York, NY: 5th Edition. 1999; 1039-1051.

Reconstructing complex wounds is accomplished by shifting or transferring tissues to the wound from a different part of the body.

A “skin graft” is the transfer of a portion of the skin (without its blood supply) to a wound. A “flap” consists of one or more tissue components including skin, deeper tissues, muscle and bone. Flaps are transferred with either their own, original blood supply (pedicle flap) or with detached blood vessels which are attached at the site of the wound (free flap).

Skin grafts survive as oxygen and nutrients diffuse into them from the underlying wound bed. Long term survival depends on a new blood supply forming from the wound to the graft. When the wound bed does not have enough oxygen supplied to it, the skin graft will at least partially fail. Common causes for this are previous radiation to the wound area, diabetes mellitus, and certain infections. In these situations, the availability of oxygen in the wound bed can be increased with hyperbaric oxygen therapy (HBO2) in preparation for skin grafting. Additionally, HBO2 can be used after skin grafting to increase the amount of the graft that will survive in these compromised settings.

Flaps also require oxygen and nutrients to survive. The outer, visible portion (usually skin) is furthest from the source of blood supply for the flap. This is the area most likely to be compromised by inadequate oxygen. Factors such as age, nutritional status, smoking, and previous radiation result in an unpredictable pattern of blood flow to the skin. If a flap is found to have less than adequate oxygen after it has been transferred, HBO2 can help minimize the amount of tissue which does not survive and also reduce the need for repeat flap procedures.

Partial or complete failure of the wound reconstruction is very difficult for a patient and also very expensive. HBO2 can help by assisting in the preparation and salvage of skin grafts and compromised flaps.

References

1. McFarlane RM, Wermuth RE. The use of hyperbaric oxygen to prevent necrosis in experimental pedicle flaps and composite skin grafts. Plast Reconstr Surg 1966;37:422-430.
2. Greenwood TW, Gilchrist AG. The effect of HBO on wound healing following ionizing radiation. In: Trapp WC, ed. Proceedings of the Fifth International Congress on Hyperbaric Medicine, Vol 1. Barnaby, Canada: Simon Frasier University, 1973:253-263.
3. Tan CM, Im MJ, Myers RA, Hoopes JE. Effect of hyperbaric oxygen and hyperbaric air on survival of island skin flaps. Plast Reconstr Surg 1974;73:27-30.
4. Zamboni WA. Applications of hyperbaric oxygen therapy in plastic surgery. In: Oriani G, Marroni A, Wattel F, eds. Handbook on Hyperbaric Oxygen Therapy. New York: Springer-Verlag, 1996.

Thermal burn injuries, if not fatal, can cause disastrous long-term physical and emotional disability for the survivor.

Especially in closed space fires, thermal and smoke (products of combustion) damage to the lungs can occur, requiring in some cases intubation and use of a mechanical ventilator. Burn injuries characteristically progress to become deeper and more extensive with time.

Peak damage occurs within 3-4 days after the initial burn, and can be up to 10 times worse than the initial burn injury. In more severe and/or extensive burns (deep second, third and fourth degree burns), multiple aggressive surgeries are generally necessary to excise the burned tissue and later perform skin grafts to cover these areas. Burn injuries can result in lifelong difficulties, physical limitations, loss of job and employment opportunities, and significant disfigurement as the body heals from the injury.

In many cases, the burn victim's life is radically changed, literally overnight. The psychiatric adjustments can be overwhelming. When possible, these injuries should be treated in centres that specialise in the management of thermal burns.

Adjunctive hyperbaric oxygen (HBO2) therapy has been shown to limit the progression of the burn injury, reduce swelling, reduce the need for surgery, diminish lung damage, shorten the hospitalization, and result in significant overall cost savings. These benefits are more apparent if therapy is initiated within 6-24 hours of the burn injury. Ideally, the patient should have 3 sessions in the first 24 hours, twice daily treatments until the process stabilizes, then continued therapy as indicated for healing enhancement and to support grafted areas. Indications for HBO2 therapy typically include deep second-degree and third-degree burns that involve greater than 20% of the total body surface area, and less extensive burns that involve the face, hands or groin area.

Best results are realized when HBO2 is used as an integral part of an aggressive multidisciplinary approach to the management of this potentially fatal injury. HBO2 is a very safe therapy even in seriously injured patients when administered by those thoroughly trained in HBO2 therapy in the critical care setting and with appropriate monitoring precautions.

References

1. Cianci P, Lueders HW, Lee H, Shapiro RL, Sexton J, Williams C, Sato R. Adjunctive hyperbaric oxygen therapy reduces length of hospitalization in thermal burns. J Burn Care Rehabil 1989; 10: 432-435.
2. Cianci P, Sato R. Adjunctive hyperbaric oxygen therapy in treatment of thermal burns: a review. Burns 1994;20(1):5-14.
3. Cianci P, Lueders H, Lee H, Shapiro R, Sexton J, Williams C, Green B. Adjunctive hyperbaric oxygen reduces the need for surgery in 40-80% burns. J Hyper Med 1988;3:97.
4. Cianci P, Williams C, Lueders H, Lee H, Shapiro R, Sexton J, Sato R. Adjunctive hyperbaric oxygen in the treatment of thermal burns - an economic analysis. J Burn Care Rehabil 1990;11:140-143.

The Slark Hyperbaric Unit (SHU), located in Devonport, Auckland, was officially opened by the Rt. Hon. Warren Cooper in 1990.

Named after the late Royal New Zealand Navy Surgeon Commodore Tony Slark, who was a pioneer in diving medicine research, our unit brings over 40 years of diving and hyperbaric medicine knowledge and experience to New Zealand's diving community. Without doubt, this unit will continue to be at the forefront in hyperbaric medicine expertise. 

Specifications:

Weight:                                               13000 kg
Number of Compartments:                 2
Material Chamber is made from:        Steel
Interior diameter:                                2150 mm
Length of the whole chamber:            6616 mm

Main compartment length:                 3240 mm
Operating pressure:                             8.5 ATA

Max treatment depth:                          75m

People in the Chamber (not including staff)
Lying down:                                         1 patient
Seated:                                                4 patients