Frans J. Cronje, MBChB (Pret) MSc


THE DEVELOPMENT OF HYPERBARIC OXYGEN THERAPY IN SOUTH AFRICA


Hyperbaric oxygen therapy (HBO) was introduced into South Africa in the early 1960’s
1. Vickers monoplace radiotherapy chambers were acquired by three of the major State Hospitals: Groote Schuur (Cape Town), Addington (Durban) and National Hospital (Bloemfontein). HBO was originally used only as a radio-enhancer in these facilities but eventually, as this application fell into disfavor, the empirical treatment of radionecrosis, sepsis and selected problem wounds became more prevalent. Pretoria Academic Hospital purchased a Vickers hyperbaric bed in 1961 that was used for the treatment of gas gangrene, osteomyelitis, septic non-union and problem wounds for many years before it was damaged and scrapped. A local private company installed the Vickers chambers and provided the original training. This was quite rudimentary and only involved the basic operation of the equipment and fundamental safety issues. Nurses and radiotherapists mostly administered hyperbaric treatments with no requirement for medical supervision. Johannesburg General Hospital also eventually bought two Vickers clinical hyperbaric systems around 1978. One of these chambers was destroyed in a chamber fire of uncertain origin, fortunately with no loss of life. This accentuated the need for better standards. The other chamber fell into disuse by 1986. Of the seven original Vickers chambers, only one is still in operation in its original form in Bloemfontein. This chamber still treats approximately 48 patients per year with a total of 1400 over the past 30 years. Three of the remaining chambers were subsequently purchased and refurbished by a private company promoting HBO in South Africa. In March 1998 they were installed in a private hospital in Pretoria: the first private HBO facility in South Africa to date. Since then further private HBO facilities have opened in Pretoria, Durban, Cape Town and Welkom.

In 1965, the South African Navy installed a small 1,5 meter diameter Draeger multiplace recompression chamber at the Institute for Aviation Medicine in support of its two altitude chambers. It was mainly used to treat occasional divers with DCI as well as ad hoc cases of multiple sclerosis and radionecrosis. From 1993, under direction of the author, this facility started providing a regular hyperbaric therapy service. The chamber was eventually replaced by a larger, 1,8 meter diameter (6 foot), six-man chamber in April 1996. This locally constructed facility, nicknamed “Miss Piggy”, spearheaded the modern evolution of clinical hyperbaric therapy in South Africa.

In 1992 the Southern African Undersea and Hyperbaric Medical Association (SAUHMA) was formed by a group of physicians with an interest in diving and hyperbaric medicine. SAUHMA affiliated to the Undersea & Hyperbaric Medical Society (UHMS) in 1994 and has played an increasingly important role in establishing medical and safety standards for HBO in South Africa. The Association has followed the UHMS safety and medical recommendations and supports the UHMS HBO Committee’s list of indications. Next year the Association will be hosting its 7
th biennial International Conference and the 2011 ICHM conference in Cape Town will be run in conjunction with the 9th SAUHMA Conference.

The Institute for Maritime Medicine – part of the South African Military Health Service – developed the original training for physicians in diving and hyperbaric medicine in South Africa in 1972 – the Diving and Submarine Medicine Course. As its focus was primarily diving medicine, a clinical hyperbaric medical training programme was developed subsequently by the author at the Institute for Aviation Medicine in 1997: the Diving and Hyperbaric Medicine Staff Training Course (DHMSTC). Over the past 16 years, this program has been presented more than 18 times in South Africa as well as in Namibia, Cyprus, Bahrain and Thailand. The course is aimed at training physicians, nurses, emergency medical technologists and chamber technicians in clinical HBO. The course has been approved for 53 hours of CME by the UHMS is one of the designated hyperbaric medicine training programs. It was also accepted by the National Board of Diving and Hyperbaric Medical Technology (NBDHMT) as meeting the minimum academic requirement for the Certified Hyperbaric Technologist (CHT) examination.

In 2000, under guidance of Francois Burman, a mechanical engineer, and SAUHMA, the South African Bureau of Standards published a safety and quality standard for clinical HBO facilities in South Africa. This is a singular achievement and offers confidence that minimum safety and training standards will be maintained in future.

In 2003 the University of Stellenbosch (near Cape Town) established a division of underwater and hyperbaric medicine within the Department of Community Health. Under the leadership of Dr W.A.J.(Jack) Meintjes, the University has developed BScMedSc (Hons) courses in diving and hyperbaric medicine that met the training standards of the Diving Medical Advisory Committee (DMAC); the European Diving Technical Committee (EDTC); the European Committee for Hyperbaric Medicine (ECHM); and the European College of Baromedicine (ECB). Although still awaiting final approval from the National Department of Education, the University’s MSc and DSc / PhD programmes are likely to commence in 2013. Currently a comprehensive web-based post graduate education program in diving and hyperbaric medicine is also being developed by Dr Meintjes and the author, together with the ECHM and the ECB. The program will be available worldwide through already known channels such as the Oxynet Website (
www.oxynet.org) and will meet the current European Standards for Post Graduate Education in Diving and Hyperbaric Medicine

Over the past 20 years, HBO has continued to grow in acceptance and application in South Africa. Although funding through medical aids continues to be challenging, the growing familiarity and judicious use of the modality has established growing support to the extent that it is again resident in the academic hospitals of Pretoria, Stellenbosch and Bloemfontein. HBO remains a Prescribed Minimum Benefit in the Medical Schemes Act for the treatment of gas gangrene
2.

WHAT IS HBO AND HOW DOES IT WORK?


Hyperbaric oxygen therapy (HBO) is the use of 100% oxygen, breathed under pressure and delivered to the tissues by the circulation to achieve a therapeutic benefit. Under hyperbaric conditions oxygen attains medicinal properties with time and pressure providing the specific “dose” and “tissue level” required to achieve the effect. HBO provides a pressure-related increase in plasma-borne oxygen. This increases total blood oxygen content by 20 – 25% 3 and markedly improves free (i.e. dissolved) oxygen delivery to tissues, increasing the diffusion distance from the capillaries into tissues several fold 4. At these increased tissue levels, oxygen initiates a series of distinct physiological and pharmacological effects. The therapeutic range for oxygen therapy is an inspired oxygen partial pressure (piO2) of 1,5 to 3 times atmospheric pressure (ATA). Higher oxygen pressures (>3 ATA) are too toxic for clinical use. There are five groups of therapeutic mechanisms attributed to hyperbaric oxygen use:


1. Hyperoxygenation

Even under normal air-breathing conditions hemoglobin is almost fully saturated with oxygen, but a small, biologically active amount of dissolved oxygen in the plasma increases significantly and proportionally to an increasing inspired oxygen pressure. Under standard treatment pressure (2,5 ATA) the delivery of dissolved oxygen to body tissues is increased from 0,3ml O 2 per 100ml of blood to 5,5ml O 2 per 100ml blood – enough to sustain life temporarily even without hemoglobin 5. Arterial blood gas values exceed 2000 mmHg (263 kPa) paO2 under these conditions 6. HBO therefore not only adds a greater amount of “free” oxygen to the blood, but also establishes a steep diffusion gradient from the capillaries, driving the oxygen further into the tissues 7. It is to be emphasized that this oxygen must be carried by the circulation from the lungs to the tissues 8. Hyperbaric oxygen therapy does not presume absorption of oxygen through the skin.

2. Vasoconstriction

HBO causes pre-capillary vasoconstriction in non-ischaemic tissues, leaving the capillaries in ischaemic areas unaffected
9. This results in reduced hydrostatic pressure in the capillaries, with less fluid extravasation, while hyper-oxygenation continues. In the venules interstitial fluid is absorbed, the end result being a rapid and significant reduction in oedema 10. This has important implications, particularly in trauma and burns.

3. Neovascularisation (Angiogenesis)

A steep oxygen gradient between normal and abnormal tissues is a fundamental stimulus to angiogenesis
11. In some abnormal tissues (irradiated, diabetes, etc. ), the gradient is so shallow that there is little stimulus breathing air of even 100% oxygen at 1 ATA. HBO however, accentuates the oxygen gradient sufficiently to stimulate angiogenesis in these tissues 11, 12. As a result, neovascularisation (granulation tissue formation) is enhanced in these abnormal tissues while normal tissues are unaffected. The microvascular revascularization is long-lasting and affords durable results 12.

4. Altered Cell Function

HBO has several effects on the cellular components involved in wound healing. Normal tissue oxygen levels are necessary for healing to occur. HBO therapy, even once a day, has been shown to significantly improve healing in chronic ulcers
13. The intermittent periods of hyperoxia result in extended periods of normal cell function: Periods of tissue hypoxia between treatments encourage the production of cytokines 14, which stimulate healing, whereas the cellular response to these cytokines is again oxygen-dependent 15. This effect related to alternating hypoxia and normoxia is called the “oxygen paradox”. Leukocyte defense mechanisms are largely oxygen dependent 16. Phagocytosis is anerobic, but large quantities of molecular oxygen are necessary for bactericidal activity 17. Work by Knighton and Hunt has demonstrated that breathing 45% oxygen is as effective as ampicillin in controlling certain aerobic bacterial inoculations, by stimulating leukocyte function 18. In addition to the cellular effects, HBO also enhances the efficacy of certain antibiotics (e.g. penicillins, aminoglycocides, vancomycin, and clindamycin) without increasing their toxicity 19. Fibroblasts cannot produce collagen aerobically and the tensile strength of collagen (cross-linking) is also oxygen dependent 20. Leukocyte adherence to venules is an important pathophysiological mechanism in ischemic reperfusion complications that leads to the no-reflow phenomenon. HBO inhibits leukocyte endothelial adherence for a period of 12 hours after one treatment without impairing leukocyte response to infection 21. In the case of fractures, tissue hypoxia may result in cartilage formation instead of bone, predisposing to delayed or non-union 22. HBO, if applied early, appears to preferentially stimulate bone formation 23.

5. Pressure and Gas Gradients

In arterial gas embolism or decompression sickness, as may be seen in compressed gas or SCUBA divers, an increase in ambient pressure reduces the diameter of inert gas bubbles, lessening their obstructive effects
24. By breathing oxygen at pressure, the steep gas gradients promote inert gas elimination, ischaemic or hypoxic complications are reduced, and cerebral or spinal oedema is reduced by selective vasoconstriction 25.
HOW IS HBO PROVIDED?

HBO therapy requires a pressure vessel suitable for human occupancy also called a “hyperbaric chamber”.
Multiperson- or multiplace chambers are usually large metal cylinders or rectangular compartments that are pressurized with air. The whole patient is pressurized inside the chamber and breathes oxygen by means of a mask, head tent or endotracheal tube. Oxygen delivery is usually interrupted to provide “air breaks” during treatments, thereby reducing the risks for cumulative oxygen toxicity.
Single person- or monoplace chambers are small, transparent tubes that are pressurized with oxygen or air. When pressurized with oxygen, there is no need for the complex oxygen delivery systems in unventilated patients. However, by using pure oxygen inside the chamber, there is a greater risk of fire and stringent precautionary measures must be adhered to. Air breaks are provided by a demand valve and oronasal mask. In recent years, compression on air has become increasingly popular to reduce the risk of fire. Although no physical patient contact is possible during therapy, mechanical ventilation, invasive and non-invasive monitoring, intravenous infusion, and drug administration and can be performed safely and effectively with the necessary ancillary devices.
The use of oxygen under pressure has been likened to it acting as a drug, with implicit factors such as indications, dose, length of use, effectiveness, contra indications and complications
26.

WHICH CONDITIONS ARE TREATABLE WITH HBO

The Southern African Undersea and Hyperbaric Medical Association (SAUHMA) follows the recommendations of the United States based UHMS with regard to appropriate and ethical indications for the administration of HBO. UHMS is an international peer review and scientific authority of more that 2 500 scientists and clinicians which standardizes therapy and validates indications with the most up to date literature. UHMS recognizes 14 evidence-based indications for HBO at the present time (2013) 27. These are:


            WHICH PROTOCOLS ARE USED AND WHAT OUTCOMES MAY BE ANTICIPATED?

            The most common and important indications for HBO are chronic radiation damage and diabetic infections diabetic infections unresponsive to conventional care. Cochrane reviews are available for both of these as well as several other HBO indications. We will not be presenting data on decompression illness and arterial gas embolism as these are uncontested primary indications for HBO. CO poisoning is either occupational or self-inflicted in most cases and both are relatively rarely referred for HBO in South Africa. This leaves the following indications for discussion:

            1. Arterial Air / Gas Embolism (AGE)

            AGE is the result of extraneous gas -- vascularised through iatrogenic or traumatic means -- resulting in neurological deficit or death. The range of iatrogenic causes for AGE are varied and multiple. They include: neurosurgery, cardiac- and cardiopulmonary bypass surgery, coronary angioplasty, open heart surgery, arthroplasty, arthroscopy, total hip replacement, endoscopy, thoracoscopy, liver transplants, intra-aortic balloon rupture, caesarean section, laser usage, invasive monitoring, contrast studies, lung biopsy and arterialised intravenous gas embolisation. It may also occur as result of lung barotrauma due to breath holding during an underwater ascent after breathing from a compressed air source (e.g. SCUBA diving, escape from a submerged vehicle or even breathing from an inverted bucket in a domestic swimming pool). As the condition is quite rare, the diagnosis is often missed or confused with an acute stroke when patients present with neurological deficits after these procedures or incidents. Although HBO should be commenced as soon as possible, it is important to realise even delayed treatment of an arterial gas embolism with HBOT is still effective. Good neurological outcomes have been reported with HBOT many hours or even several days after an episode of gas embolism. Initial delay in recognition should therefore not be a reason to defer transfer to a hyperbaric unit, as long as this can be undertaken without compromising the patient’s care.
            In modern hyperbaric practice, pressurisation to 6 ATA (i.e. according to US Navy treatment table 6A) is rarely used and may only be indicated in exceptional cases received very shortly after onset. Usually HBOT is initiated at 2,8 ATA for 4h45 (i.e. according to U S Navy Treatment table 6) and thereafter continued twice daily for 90 minutes at 2,4 ATA to a maximum total of 10-14 treatments.

            2. Carbon Monoxide Poisoning

            Carbon monoxide poisoning due to occupational or environmental exposure is a significant cause of morbidity and mortality in the USA. It is believed to be largely undetected in the South African population at risk. The pathophysiology of CO-poisoning is not only a toxic anaemia by the formation of non-oxygen-carrying carboxyhaemoglobin. CO also causes mitochondrial cytochrome disruption, initiates neuronal lipid peroxidation and causes ischaemia-reperfusion-type injuries. These combined pathophysiological mechanisms not only put the patient at immediate risk, but also contribute to delayed neurological sequelae in a significant number of survivors due to destruction of specific neuronal structures. Detection of carboxyhaemoglobin (COHb) is sometimes unreliable after prolonged oxygen breathing and COHb levels do not always correlate well with the severity or prognosis of the patient. Some authors feel that subtle but significant neurological abnormalities are often missed and recommend that simple psychometric testing be performed routinely in the acute stage. This has been found to be a more sensitive and specific indicator of significant CO intoxication and is also an indication for HBOT.
            The logical use of hyperbaric oxygen therapy has been borne out by several clinical studies comparing outcomes. These indicate that patients with suspected carbon monoxide poisoning who are pregnant; have lost consciousness during the course of intoxication; have detectable psychometric or neurological abnormalities on admission; have electrocardiographical changes;
            or have a verified carboxyhaemoglobin level above 25%, should be referred for HBOT as soon as possible. Treatments are commenced at 3 ATA for 90 minutes. More than two or three treatments are rarely required, making HBO very cost-effective.

            3. Clostridial Myositis & Myonecrosis (Gas Gangrene)

            This is the classic indication for hyperbaric oxygen in combination with conservative surgery and antibiotics. When used early (i.e. within 24 hours of diagnosis), and before ablative surgery, HBO reduces morbidity and mortality significantly
            28. Tissue and limbs can often be spared and spread to the trunk, which carries a high mortality, can be avoided. HBO terminates the production of alpha toxin, the lethal element of gas gangrene, within minutes and prevents ongoing liquefaction of tissue 29. The need for extensive debridement or amputation is thereby significantly reduced. Following HBO, along with resuscitation and antibiotics, patients are in a better state for surgery, and, important for the surgeon, the demarcation between viable and non-viable tissue is more distinct, thereby avoiding over-excision of tissue in the initial stages 28, 29.

            4. Crush Injury, Compartment Syndrome and Other Acute Traumatic Ischemias

            Crush injuries, compartment syndromes, thermal burns, compromised flaps and tissue replantations share a number of pathophysiological processes that benefit from adjunctive HBO. In all these injures a gradient of injury exists, ranging from viable to non-viable tissue. Secondary pathophysiological events, e.g. hypoxia, ischemia, edema, reperfusion injury, and sepsis shift the gradient towards further tissue loss. Hyperbaric oxygen, if introduced early, improves outcome, by reducing the effects of ischemia and hypoxia and reducing oedema and necrosis as confirmed clinically in a recent prospective, randomized, double blinded and placebo controlled trial by Bouachour et al
            30. Here HBO was able to limit the number of repetitive surgical procedures in relation to severe limb trauma. Patients over 40 years of age with Gustillo grade III soft tissue injuries should receive adjunctive HBO if available.

            5. Decompression Sickness (DCS)

            HBOT is the unchallenged primary treatment for DCS. The increased pressure reduces bubble size while the oxygen establishes a favourable diffusion gradient to rapidly eliminate the inert gas from the bubbles and provide oxygenation to ischaemic and hypoxic tissues. There is no alternative definitive therapy. In the emergency situation the administration of 100% oxygen and isotonic fluids (normal saline or Ringers Lactate) form the cornerstones of management. As in the case of an arterial gas embolism, recompression treatment should not be deferred in delayed cases. Delays of 36 to 72 hours or longer are common in diving injuries, and HBOT is still of great benefit at that time: It is never too late to recompress.
            The Divers Alert Network (DAN) is an independent non-profit organisation that provides a 24-hour emergency hotline for injured divers. DAN’s services are available to assist healthcare professionals in getting immediate access to dive medical expertise and recompression facilities all over the world. DAN’s services to recreational divers include dive safety education, training in oxygen administration, as well as emergency evacuation and treatment for diving injuries and dive medical insurance. These services can assist greatly in the management of a diving casualty. DAN’s global membership exceeds 170 000 divers, making it the largest organisation of recreational divers. Five International DAN (IDAN) systems are now in place: DAN America, DAN Europe, DAN Japan, DAN Southeast Asia Pacific and since 1996, DAN Southern Africa. For assistance with a diving casualty, contact DAN’s 24-hour hotline at +27(0) 11 242-0112 or 0800 020111 (toll-free within South Africa) or 112 on the MTN cell phone network. For general information, contact DAN’s help line at (011) 242-0382 or share-call: 086-0242 242 or visit the DAN Southern Africa and IDAN website at www.dansa.org.

            6. Arterial Insufficiencies
            Several surgical conditions share arterial insufficiency as a common pathophysiological feature. HBO may be a suitable therapy when the insufficiency is either
            acute and transient (e.g., thrombotic, embolic, traumatic or in an ischemia-reperfusion / revascularization / reimplantation setting) or chronic and relative (i.e., where a temporary increase in oxygen demand causes a relative shortage in supply – such as surgical wounding or pressure ulceration in a chronic ischemic tissue). Two conditions are defined specifically within this category:
            a. Selected Wound Care

            “Problem wound” implies wounds which fail to respond adequately and timeously to conventional treatment. This includes certain arterial insufficiency ulcers, venous insufficiency ulcers, diabetic wounds and infections, chronic radiation necrosis and decubitus ulcers. Of all the factors involved in healing, oxygen is the most important variable. Tissue hypoxia predisposes to decreased fibroblast proliferation, poor collagen production and cross-linking, impaired leukocyte function and decreased angiogenesis (granulation tissue formation). HBO restores a favorable milieu in which healing and antibacterial mechanisms again become functional or are enhanced. While bypass surgery or angioplasty are more definitive in treating arterial insufficiency ulcers, certain subgroups benefit from adjunctive HBO: These include patients whose wounds do not respond adequately after successful bypass surgery (e.g. diabetics); patients who are inoperable or unsuitable for vascular surgery but are shown to have adequate transcutaneous oximetry values 31; patients with residual or refractory soft tissue or bone infection; and patients with doubtful long term graft patency who require expedient wound healing. In these cases HBO is often the only remaining solution for success. Transcutaneous oximetry provides a specific and sensitive way of measuring actual tissue oxygenation; it thus provides a reliable means of patient selection and prediction of healing failure in the abovementioned cases 32, 33.
            In infected diabetic foot wounds and gangrene, HBO has been shown to be effective by a number of authors
            34, 35, 36, 37, 38. Patients with Wagner grades III (deep infection) and IV (fore-foot gangrene) foot infections derive significant benefits from HBO (with appropriate vascular interventions when indicated): Oriani et al confirmed a significant reduction in below-knee amputation rates in HBO treated patients (5% vs 33%) compared to matched controls 34. Similarly Cianci et al achieved 85% long term (average 54 months) limb salvage rates 35. For HBO to be of value, transcutaneous oximetry values should confirm adequate oxygen delivery to the affected areas (450 mm Hg pO2 at 2,5 ATA) 38, 39. For best results, HBO should be combined early in the management of these patients.
            Venous insufficiency ulcers rarely require HBO. Attention to the basic pathology indicates appropriate therapy, including surgery if necessary, to the venous system, along with compression bandaging. However HBO, as a stimulus for granulation tissue formation, is of value in the preparation and support of grafting of extensive or intractable ulcers
            13. Decubitus ulcers are primarily managed with good wound care. However HBO should be considered in cases with concomitant osteomyelitis, progressive necrosis or reconstruction problems 27.

            4. Severe Anemia

            In exceptional blood loss anemia or certain hemolytic anemias where transfusion is not possible or inappropriate (e.g. Jehovah’s Witnesses), the intermittent use of HBO dissolves enough oxygen in the plasma to support basic metabolic needs
            5. This can be continued together with aggressive erythropoietin therapy until the body has produced sufficient red blood cells 27.

            5. Necrotising Soft Tissue Infections

            As an adjunct to surgical debridement and systemic antibiotics, HBO directly inhibits anaerobic bacterial growth and indirectly improves the body’s response to aerobic infections by potentiating white cell bacterial killing 40. The principle treatment remains surgical debridement and antibiotics, but HBO is of use in high risk (e.g. perineal and truncal infections) or poorly responding patients. Riseman and Zamboni obtained a mortality reduction from 66% to 23% in such cases, with considerably less debridement required 41. Hollabaugh, in a recent study on Fournier’s gangrene, demonstrated a nine fold reduction in mortality in matched, randomised patients 42. If the progression of the disease is not arrested with adequate surgery and antibiotics within 48-hours, patients should be referred for HBO if possible.

            6. Osteomyelitis (Refractory)

            Chronic osteomyelitis is considered to be refractory when it has persisted or recurred after appropriate interventions. These normally consist of surgical debridement and a prolonged course of organism specific antibiotics. Mader, one of the authors of the international Cierny-Mader classification of chronic osteomyelitis, recommends that HBO be added to standard treatment regimens for localized and diffuse osteomyelitis in compromised hosts, e.g. diabetic, elderly, chronically hypoxic, malnourished patients or smokers
            43, 44. Only HBO is able to increase medullary bone oxygen tensions, thereby improving leukocyte bactericidal activity, potentiating antimicrobials without increasing their toxicity or side effects, increasing collagen production and angiogenesis, and improving osteoclast function with subsequent removal of necrotic bone 45, 46. The high morbidity, mortality and limited surgical options for managing malignant otitis externa as well as osteomyelitis of the sternum, cranium and vertebrae, justify the early inclusion of HBO in their management 27.

            7. Radionecrosis

            Radiation produces a dose related, gradual but progressive obliterative endartritis and cellular dysfunction, leading to hypoxic, hypovascular and hypocellular tissue
            12. This tissue is vulnerable to trauma and unable to heal due to an imbalance between oxygen supply and demand. This results in a non-healing wound, in which the metabolic demands for healing and homeostasis exceed the oxygen and vascular supply 12. HBO has the unique ability to reverse some of the cellular changes and restore microvascular density to within 75 to 85% of normal 12, 47. This restores the tissue’s ability to heal and affords surgical and reconstructive options not otherwise available or reliable. In patients at risk for developing mandibular osteoradionecrosis (ORN), or those with established ORN, HBO is of significant value when it is provided before surgery is undertaken 48, 12. Previous treatment failures reported in early South African literature, were the result of inadequate surgery following preparatory HBO 49. HBO alone cannot resolve established ORN without subsequent sequestrectomy to bleeding bone.

            HBO is also of value in the prevention and treatment of soft tissue radionecrosis and is recommended pre and post-operatively in relation to elective surgery in irradiated tissues
            50. In addition, HBO has been shown to be an effective primary treatment for refractory hemorrhagic radiation cystitis 51.

            8. Compromised Skin Grafts, Flaps and Reimplantations

            Lack of granulation tissue limits plastic surgical options. HBO, by creating steep oxygen gradients, is a powerful stimulus for angiogenesis and fibroplasia
            11, 12, 14, 52. HBO may be indicated when granulation tissue is lacking, either to achieve healing by secondary intention or in preparation for grafting 13. Early application of HBO is associated with improved tissue salvage in compromised flaps 53 HBO can improve flap survival and extend the margins of viable tissue while reducing the risk of sepsis 15, 16, 17. While revision of vascular anastomoses is required for inflow obstruction, HBO is able to attenuate the ischemia reperfusion process that would follow reflow. Flap mottling after surgery is therefore an important emergent indication for HBO 54. Similarly, in limb or tissue loss followed by reimplantation, HBO attenuates ischemia-reperfusion, supports the avulsed or degloved tissue after reattachment, and stimulates angiogenesis and healing 55.

            9. Thermal Burns

            HBO in burns has the ability to maintain microvascular integrity, reduce local and systemic oedema and minimize propagation of the burn into adjacent and subjacent tissues
            56. Mortality, hospital stay and graft requirements are positively affected 57, 58. Epithelialisation is also promoted, thereby reducing the incidence of contractures as a time-course related complication 58. HBO is able to prevent partial thickness burns from becoming full thickness if applied early 59.

            HBO is not a substitute for established burn care but is a useful adjunct if applied early. Out of facility transfers are not indicated, but patients with 20-80% burns or burns affecting vital areas should receive HBO within the first 24-hours if this is available in-house
            60. 31% of burn units in the USA routinely use HBO as part of their treatment regimens. Standard resuscitation and burn care must be continued in the hyperbaric environment 60.

            10. Intracranial Abscess

            The clinically observed beneficial effects of HBO in the management of intracranial abscess are derived from direct inhibition of the predominantly anaerobic organisms, the reduction of perifocal oedema, enhancement of host defense mechanisms and adjunctive efficacy in resolving concomitant skull osteomyelitis
            61. Morbidity and mortality in multifocal and inoperable brain abscesses appears to be significantly reduced in patients receiving HBO when compared to conventional care only 61.


            COCHRANE ANALYSES ON THE USE OF HBO IN RADIATION TISSUE INJURY AND WOUND CARE

            RADIATION TISSUE INJURY

            ID: CD005005
            AU: Bennett MH, Feldmeier J, Hampson N, Smee R, Milross C
            TI:
            Hyperbaric oxygen therapy for late radiation tissue injury
            SO: Bennett MH, Feldmeier J, Hampson N, Smee R, Milross C. Hyperbaric oxygen therapy for late radiation tissue injury. The Cochrane Database of Systematic Reviews: Reviews 2005 Issue 3 John Wiley & Sons, Ltd Chichester, UK DOI: 10.1002/14651858.CD005005.pub2
            YR: 2005
            NO: 3
            PB: John Wiley & Sons, Ltd
            US: http://www.mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD005005/frame.html
            KY: Humans [checkword]; Hyperbaric Oxygenation; Neoplasms [radiotherapy]; Osteoradionecrosis [prevention & control]; Radiation Injuries [prevention & control] [therapy]; Randomized Controlled Trials
            CC: HM-GYNAECA
            DOI: 10.1002/14651858.CD005005.pub2
            AB: BACKGROUND: Cancer is a significant global health problem. Radiotherapy is a treatment for many cancers and about 50% of patients having radiotherapy will be long-term survivors. Some will experience LRTI developing months or years later. HBOT has been suggested for LRTI based upon the ability to improve the blood supply to these tissues. It is postulated that HBOT may result in both healing of tissues and the prevention of problems following surgery. OBJECTIVES: To assess the benefits and harms of HBOT for treating or preventing LRTI. SEARCH STRATEGY: We searched The Cochrane Central Register of Controlled Trials (CENTRAL) Issue 3, 2004, MEDLINE, EMBASE, CINAHL and DORCTHIM (hyperbaric RCT register) in September 2004. SELECTION CRITERIA: Randomized controlled trials (RCTs) comparing the effect of HBOT versus no HBOT on LRTI prevention or healing. DATA COLLECTION AND ANALYSIS: Three reviewers independently evaluated the quality of the relevant trials using the guidelines of the Cochrane Handbook Clarke 2003) and extracted the data from the included trials. MAIN RESULTS: Six trials contributed to this review (447 participants). For pooled analyses, investigation of heterogeneity suggested important variability between trials. From single studies there was a significantly improved chance of healing following HBOT for radiation proctitis (relative risk (RR) 2.7, 95% confidence Interval (CI) 1.2 to 6.0, P = 0.02, numbers needed to treat (NNT) = 3), and following both surgical flaps (RR 8.7, 95% CI 2.7 to 27.5, P = 0.0002, NNT = 4) and hemimandibulectomy (RR 1.4, 95% CI 1.1 to 1.8, P = 0.001, NNT = 5). There was also a significantly improved probability of healing irradiated tooth sockets following dental extraction (RR 1.4, 95% CI 1.1 to 1.7, P = 0.009, NNT = 4).There was no evidence of benefit in clinical outcomes with established radiation injury to neural tissue, and no data reported on the use of HBOT to treat other manifestations of LRTI. These trials did not report adverse effects. AUTHORS' CONCLUSIONS: These small trials suggest that for people with LRTI affecting tissues of the head, neck, anus and rectum, HBOT is associated with improved outcome. HBOT also appears to reduce the chance of osteoradionecrosis following tooth extraction in an irradiated field. There was no such evidence of any important clinical effect on neurological tissues. The application of HBOT to selected patients and tissues may be justified. Further research is required to establish the optimum patient selection and timing of any therapy. An economic evaluation should be also be undertaken. There is no useful information from this review regarding the efficacy or effectiveness of HBOT for other tissues.
            PLAIN LANGUAGE SUMMARY: Hyperbaric oxygen (HBO) may improve radiation injuries of the head, neck and bowel. It also appears to reduce the chance of bone death following tooth extraction. There is a risk of serious complications developing after radiation treatment for cancer (late radiation tissue injury (LRTI). Hyperbaric oxygen therapy (HBOT) involves breathing oxygen in a specially designed chamber. It is used as a treatment to improve oxygen supply to damaged tissue and stimulate healing. We found some evidence that LRTI affecting the head, neck and lower end of the bowel can be improved with HBOT. There is little evidence for or against benefit in other tissues affected by LRTI. Our conclusions are based on six randomized trials with a limited number of patients. Further research is needed.

            WOUND HEALING

            ID: CD004123
            AU: Kranke P, Bennett M, Roeckl-Wiedmann I, Debus S
            TI:
            Hyperbaric oxygen therapy for chronic wounds
            SO: Kranke P, Bennett M, Roeckl-Wiedmann I, Debus S.
            Hyperbaric oxygen therapy for chronic wounds. The Cochrane Database of Systematic Reviews: Reviews 2004 Issue 1 John Wiley & Sons, Ltd Chichester, UK DOI: 10.1002/14651858.CD004123.pub2
            YR: 2004
            NO: 1
            PB: John Wiley & Sons, Ltd
            US: http://www.mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD004123/frame.html
            KY: Humans [checkword]; Amputation [utilization]; Chronic Disease; Diabetic Foot [therapy]; Hyperbaric Oxygenation [adverse effects]; Leg Ulcer [therapy]; Pressure Ulcer [therapy]; Randomized Controlled Trials; Varicose Ulcer [therapy]; Wound Healing
            CC: HM-WOUNDS
            DOI: 10.1002/14651858.CD004123.pub2
            AB: BACKGROUND: Chronic wounds are common and present a health problem with significant effect on quality of life. The wide range of therapeutic strategies for such wounds reflects the various pathologies that may cause tissue breakdown, including poor blood supply resulting in inadequate oxygenation of the wound bed. Hyperbaric oxygen therapy (HBOT) has been suggested to improve oxygen supply to wounds and therefore improve their healing. OBJECTIVES: To assess the benefits and harms of adjunctive HBOT for treating chronic ulcers of the lower limb (diabetic foot ulcers, venous and arterial ulcers and pressure ulcers). SEARCH STRATEGY: We searched the Cochrane Wounds Group Specialized Trial Register (searched 6 February 2003), CENTRAL (The Cochrane Library Issue 1, 2003), Medline (1966 - 2003), EMBASE (1974 - 2003), DORCTHIM (1996 - 2003), and reference lists of articles. Relevant journals were handsearched and researchers in the field were contacted. SELECTION CRITERIA: Randomized studies comparing the effect on chronic wound healing of therapeutic regimens which include HBOT with those that exclude HBOT (with or without sham therapy). DATA COLLECTION AND ANALYSIS: Three reviewers independently evaluated the quality of the relevant trials using the validated Oxford-Scale (Jadad 1996) and extracted the data from the included trials. MAIN RESULTS: Five trials contributed to this review. Diabetic foot ulcer (4 trials, 147 patients): Pooled data of three trials with 118 patients showed a reduction in the risk of major amputation when adjunctive HBOT was used, compared to the alternative therapy (RR 0.31, 95% CI 0.13 to 0.71). Sensitivity analysis for the allocation of dropouts did not significantly alter that result. This analysis predicts that we would need to treat 4 individuals with HBOT in order to prevent 1 amputation in the short term (NNT 4, 95% CI 3 to 11). There was no statistically significant difference in minor amputation rate (pooled data of two trials with 48 patients). Healing rates were reported in one trial (Abidia 2003) which showed a significant improvement in the chance of healing 1 year after therapy (RR for failure to heal with sham 2.3, 95%CI 1.1 to 4.7, P=0.03), although no effect was determined immediately post HBOT, nor at 6 months. Further, the beneficial effect after 1 year was sensitive to allocation of dropouts. Venous ulcer: (1 trial, 16 patients): This trial reported data at six weeks (wound size reduction) and 18 weeks (wound size reduction and healing rate) and suggested a significant benefit of HBOT in terms of reduction in ulcer area only at 6 weeks (WMD 33%, 95%CI 19% to 47%, P<0.00001). Arterial and pressure ulcers: No trials that satisfied inclusion criteria were located. AUTHORS' CONCLUSIONS: In people with foot ulcers due to diabetes, HBOT significantly reduced the risk of major amputation and may improve the chance of healing at 1 year. The application of HBOT to these patients may be justified where HBOT facilities are available, however economic evaluations should be undertaken. In view of the modest number of patients, methodological shortcomings and poor reporting, this result should be interpreted cautiously however, and an appropriately powered trial of high methodological rigor is justified to verify this finding and further define those patients who can be expected to derive most benefit from HBOT. Regarding the effect of HBOT on chronic wounds associated with other pathologies, any benefit from HBOT will need to be examined in further, rigorous randomized trials. The routine management of such wounds with HBOT is not justified by the evidence in this review.
            PLAIN LANGUAGE SUMMARY: We found some evidence that people with diabetic foot ulcers are less likely to have a major amputation if they receive hyperbaric oxygen therapy. This is based on three randomized trials with a limited number of patients. Further research is needed. Chronic wounds, often associated with diabetes, arterial or venous disease are common and have a high impact on the well-being of those affected. Hyperbaric oxygen therapy (HBOT) is a treatment designed to increase the supply of oxygen to wounds that are not responding to other measures to treat them. HBOT involves people breathing pure oxygen in a specially designed chamber (such as that used for deep sea divers suffering pressure problems after resurfacing).The review of trials found that HBOT seems to reduce the number of major amputations in people with diabetes who have chronic foot ulcers, and may reduce the size of wounds caused by disease to the veins of the leg, but found no evidence to confirm or refute any effect on other wounds caused by lack of blood supply through the arteries or pressure ulcers.


            DANGERS, SIDE EFFECTS AND SPECIAL PRECAUTIONS

            The most common problem is barotrauma of the middle ear. Patients are taught auto-inflation techniques and sometimes decongestants are used. If necessary grommets can be inserted. In emergency treatments in unconscious patients, myringotomy is performed. Prolonged exposure to high-pressure oxygen can cause two potentially serious side-effects, seizures and pulmonary oxygen toxicity. Both of these are very rare, as safe therapeutic limits have been developed over time. Oxygen toxicity seizures are not inherently harmful, and air breathing intervals during HBO therapy are factored into treatment regimes and prophylactic vitamin E is administered to further minimize the risk
            62. Careful history is taken and prophylactic treatment is given in those with specific risk factors; e.g. those with history of seizures, fever, acidosis, or low blood sugar. Claustrophobia may be a problem with some patients, and it is reduced by having an attendant inside the chamber (multiplace) or beside it (monoplace). Mild sedatives are sometimes indicated.
            Fire risk precautions are mandatory, with unsafe objects not being admitted. Patients are expected to stop smoking for the entire course of HBO therapy. The vasoconstrictive effects of nicotine may interfere with angiogenesis, and raised carbon monoxide levels reduce the full benefit of oxygenation.


            CONTRA-INDICATIONS TO HBO

            The only absolute contra-indications are an untreated pneumothorax and certain anti-cancer drugs, i.e. doxorubicin, bleomycin and cisplatinum, as HBO significantly increases their cytotoxicity. Relative contra-indications include acute viral URTI’s, sinusitis, bullous pulmonary disease, history of spontaneous pneumothorax and congenital spherocytosis. Consultation with a physician trained in hyperbaric medicine is important, both for evaluating the indication for HBO therapy and for addressing any possible contraindications.


            SAUHMA POLICY ON THE CLINICAL APPLICATION OF HBO

            In order to provide clear lines of medical responsibility, ensure competence and safety, and establish a scientifically and financially viable basis for clinical HBO in South Africa, SAUHMA endorses four fundamental principles:

            Clinical HBO should be provided in a hospital or a registered health care facility.

            A qualified hyperbaric physician (minimum Category II, see below) must be directly responsible for all aspects of use of a pressure vessel for medical purposes, and as such must perform the following functions:
            specifically prescribe HBO for each patient
            determine if there are any risk factors or contra indications to clinical HBO
            confirm the suitability of the chamber and oxygen delivery system for each patient
            supervise the safe and competent operation of the chamber
            and ensure patient and hyperbaric staff safety
            An exception to this is the treatment of DCI in commercial and military divers, where specific diving regulations permit non-medical chamber supervisors to initiate recompression treatment.

            A qualified hyperbaric physician (minimum Category II, see below) should always be in attendance (defined as being immediately available at all times) during treatments to ensure the provisions of par. 2 are met and to deal with any medical emergencies that may arise in the chamber.

            4. An appointment of Medical Director should be made for each hyperbaric facility. The title represents the chief medical authority at a clinical hyperbaric facility (and this is referred to throughout the text). The Medical Director, in terms of the Occupational Safety Act, is also defined as the user of the equipment (refer to the section on South African Fire Standards).


            CREDENTIALLING AND TRAINING STRUCTURE

            The following credentialing and training structure has been approved by SAUHMA and is in the process of being fully implemented.


            Hyperbaric Physician Training and credentialing

            A physician practising hyperbaric medicine must have a thorough understanding of the various physiological, pharmacological, occupational, operational and safety aspects of the treatment he/she is prescribing as well as the potential risks and complications. In addition those practising as hyperbaric medicine specialists in wound care programs must also have sufficient training and experience in wound care and in the selection of patients with wounds that may benefit from adjunctive hyperbaric oxygen treatment. The minimum acceptable academic requirement for hyperbaric physicians is therefore the successful completion of at least a 50-hour hyperbaric medicine course, approved by SAUHMA and/or the UHMS as well as suitable clinical experience in the management of patients requiring recompression and/or hyperbaric oxygen therapy. "Suitable experience" can be determined and validated by the Medical Director of the hyperbaric facility they are associated with, or by SAUHMA. This should include training and experience in the therapeutic use of increased atmospheric pressure and oxygen (or gas mixtures) in the treatment of DCI, as well as in the management of other clinical conditions treated with HBO. The credentialing structure for hyperbaric physicians is as follows:

            CATEGORY I: Associate Hyperbaric Physician (AHP)

            AHP's are physicians who have had a
            minimum orientation to medical care in the hyperbaric environment and, if working in a multiplace facility, must be dive medically fit. Such physicians (e.g. specialists in Anaesthetics, Critical Care or Emergency Medicine) provide their services under the supervision of a Category II or III physician. This may involve e.g., emergency care, anaesthesia or ventilator support to patients during hyperbaric treatment. The minimum orientation may be attained by the attendance of an academic course recommended, accepted or provided by the respective hyperbaric departments. In addition, such physicians must complete any competency requirements set by the hyperbaric facility, such as an annual check-dive to 50 MSW, depending on the services provided and the equipment used by the facility (monoplace vs. multiplace).

            CATEGORY II: Hyperbaric Physician (HP)

            HP's are physicians who have successfully completed a
            minimum of 50 hours of academic training in hyperbaric and diving medicine in courses recognized by SAUHMA and/or the UHMS, and have suitable clinical experience in the management of patients requiring recompression or hyperbaric oxygen therapy (as determined by SAUHMA and/or the Medical Director of the hyperbaric facility they serve). Such physicians, if working in a multiplace facility, must be dive medically fit. They may direct routine hyperbaric medicine treatments and provide emergency hyperbaric medicine treatments in consultation with a physician holding category III clinical privileges. A category II physician is expected to request consultation or assistance when:
            Diagnosis and/or management remain in doubt over an unduly long period of time, especially in the presence of life-threatening illness.
            Unexpected complications arise which fall outside his/her level of competence and experience.
            Specialised treatment or procedures are contemplated with which he/she is not familiar.
            Mixed gas or treatment depths greater than 18 MSW are required in the treatment of DCI.
            Granting of Category II privileges is further dependent upon the specific needs of the hyperbaric medicine facility they serve as determined by the Medical Director or facility administrator.

            CATEGORY III: Hyperbaric Consultant

            Physicians with these privileges have the highest level of competence and training in hyperbaric and diving medicine on a par considered appropriate for a sub-specialist. Such training should include certification in both diving medicine and clinical HBO through:
            The Institute for Maritime Medicine (South Africa) Diving and Submarine Medicine Course or equivalent e.g., the National Oceanic and Aeronautical Administration (NOAA) Diving Medical Physician course or the Diving Medical Advisory Committee course (UK); and
            A SAUHMA and/or UHMS sponsored course (e.g. Diving and Hyperbaric Medicine Staff Training Course);
            or
            Special competency certification such as the Certified Hyperbaric Technologist's (CHT) examination through the NBDHMT
            or
            Other appropriate postgraduate training (e.g. South Pacific Undersea Medical Society Diploma or Diploma in Baromedicine).
            These physicians, if working in a multiplace facility, must be dive medically fit. Granting of Category III privileges is further dependent upon the specific needs of the hyperbaric facility they serve as determined by the Medical Director or facility administrator.

            Register of Hyperbaric Physicians

            A register is maintained of all physicians actively involved in hyperbaric medicine based on the above-mentioned structure. This adds to the credibility and recognition of hyperbaric medicine as a peer-reviewed sub-speciality and stimulates interest and growth in this field of medicine.


            Hyperbaric Nurse Training and credentialing

            The training and credentialing structure for a hyperbaric nurse has not yet been fully implemented. The South African Nursing Council (SANC) has been requested to recognize hyperbaric nursing as a valid sub-specialty. Primary nursing credentials and experience still define the scope of practice for each individual. Three categories have been accepted by SAUHMA to recognize nursing competence in the hyperbaric environment:


            CATEGORY I: Assistant Hyperbaric Nurse (AHN)

            AHN's are nurses who have had a
            minimum orientation to nursing care in the hyperbaric environment and, if working in a multiplace facility, are dive medically fit. Such nurses always function under the direct supervision of a Hyperbaric Nurse, Hyperbaric Paramedic, or as determined by the Medical Director of the hyperbaric facility they serve. The minimum orientation may be attained by the attendance of an academic course recommended, accepted or provided by their respective hyperbaric departments. These nurses usually work in hyperbaric facilities on a part-time basis and/or make themselves available for clinical support of patients with special needs e.g., intensive care or ventilator support. Such nurses must complete an annual orientation check-dive to 50 MSW or any other competency requirements depending on the services provided and the equipment used by the facility (monoplace vs. multiplace).


            CATEGORY II: Hyperbaric Nurse (HN)

            HN's are nurses who have successfully completed a
            minimum of 50 hours of academic training in clinical hyperbaric medicine through a course recognized by SAUHMA and/or the UHMS. They also have suitable clinical experience in the management of patients requiring recompression or hyperbaric oxygen treatment (as determined by SAUHMA and/or the Medical Director of the hyperbaric facility they serve). HN's, if working in a multiplace facility, must be dive medically fit. They may provide patient care during routine hyperbaric treatments, within their scope of nursing practice, as defined by the SANC. Granting of Category II privileges is further dependent upon the needs of the specific hyperbaric facility that they serve as determined by the Medical Director or facility administrator.


            CATEGORY III: Certified Hyperbaric Nurse (CHN)

            CHN's have the highest level of competence and training in hyperbaric nursing. They have successfully completed a minimum of 50 hours of academic training in clinical hyperbaric medicine through a course recognized by SAUHMA and/ or the UHMS. They have more than 480 hours of hyperbaric nursing experience and have passed the CHT exam offered by the NBDHMT, or the Certified Hyperbaric Registered Nurse (CHRN) exam offered by the Baromedical Nurses Association (BNA). Suitable experience or training in intensive care, trauma or theatre nursing is a further consideration. Such nurses, if working in a multiplace facility, must be dive medically fit. CHN's may provide patient care, during
            all types of hyperbaric treatments, within their scope of practice as defined by the SANC. Granting of Category III privileges is further dependent upon the specific needs of the hyperbaric facility they serve as determined by the Medical Director or facility administrator.


            Register of Hyperbaric Nurses

            A register is maintained of all nurses actively involved in hyperbaric medicine based on the above-mentioned categories. This adds to the credibility and recognition of hyperbaric nursing as a valid sub-speciality. It also stimulates interest and creates career opportunities within this field of nursing.


            Hyperbaric Training and credentialing for Emergency Service Personnel

            The South African nomenclature for Emergency Service Personnel differs considerably from that of the US. In the interest of the reader, and to avoid confusion with unfamiliar terms, the US classification has been used as the basis of this structure.

            There are no specific restrictions to Emergency Medical Technologists (EMT), Intermediate EMT's (EMT-I) or Paramedics providing care inside a hospital or registered health care facility in South Africa, as long as they remain within their scope of practice as defined by the South African Medical and Dental Council (MDC). The following three categories have been accepted by SAUHMA to recognize competence in the hyperbaric environment:


            CATEGORY I: Chamber Attendant (CA)

            CA's are EMT’s, EMT-I's or Paramedics that have had a
            minimum orientation to patient care in the hyperbaric environment and, if working in a multiplace facility, are dive medically fit. CA's always function under the supervision of a Hyperbaric Paramedic, Hyperbaric Nurse or as determined by the Medical Director of the hyperbaric facility that they serve. The minimum orientation may be attained by the attendance of an academic course recommended, accepted or provided by their respective hyperbaric departments. CA's generally work in hyperbaric facilities on a part-time basis. They must complete an annual orientation check-dive to 50 MSW or any other competency requirements based on the services provided and equipment used in the hyperbaric facility (monoplace vs. multiplace). CA's, who take the CHT exam, may subsequently be referred to as Certified Hyperbaric Technologists.


            CATEGORY II: Hyperbaric Paramedic (HP)

            HP's are paramedics (Note: In South Africa, the term Paramedic may only be used by Critical Care Assistants or National Diplomats in Emergency Care as defined by the South African Medical and Dental Council) who have successfully completed a minimum of 50 hours of academic training in clinical hyperbaric medicine through a course recognized by SAUHMA and/or the UHMS. HP's have suitable clinical experience in the management of patients requiring recompression or hyperbaric oxygen treatment (as determined by SAUHMA and/or the Medical Director of the hyperbaric facility they serve). Such paramedics, if working in a multiplace facility, must be dive medically fit and may provide patient care during routine hyperbaric treatments within their scope of practice, as defined by the MDC. Granting of Category II privileges is further dependent upon the specific needs of the hyperbaric facility that they serve as determined by the Medical Director or facility administrator.


            CATEGORY III: Certified Hyperbaric Paramedic

            Certified Hyperbaric Paramedics (CHP) have the highest level of competence and training in hyperbaric and diving medicine. They have successfully completed a minimum of 50 hours of academic training in clinical hyperbaric medicine through a course recognized by SAUHMA and/or the UHMS. They have more than 480 hours hyperbaric experience and have passed the CHT exam offered by the NBDHMT. These CHP’s, if working in a multiplace facility, must be dive medically fit. They may provide patient care during all hyperbaric medicine treatments within their scope of practice, as defined by the MDC. Granting of Category III privileges is further dependent upon the specific needs of the hyperbaric facility they serve as determined by the Medical Director or facility administrator.


            Clinical Hyperbaric Chamber Operators (CHCO)

            Non-medical, -nursing or -emergency service trained individuals with an interest in hyperbaric medicine may elect to qualify as CHCO by taking the Clinical Hyperbaric Chamber Operator Course (CHCOC) or equivalent training program. In rare instances, CHCO's may serve as chamber attendants at the discretion of, and under the direct supervision of the Medical Director of the hyperbaric facility. CHCO's, who have passed the CHT exam, may subsequently be referred to as Certified Hyperbaric Technologists. Any of the other professional staff categories may also qualify as CHCO's by successfully completing the appropriate course. Dual qualification offers many advantages to multiplace facilities by permitting reciprocating functions in and outside the chamber.


            COST EFFECTIVENESS OF HBO

            The author participated as a member of an expert jury for the European Committee for Hyperbaric Medicine and the European Tissue Repair Society in . Using a model for predicting the overall costs of major categories of wounds with or without HBO based on Italian Ministry of Health data and outcome data from the literature HBOT for radionecrosis and diabetic foot infections not only appears to be clinically effective, but also likely to reduce the general costs of a nation’s healthcare, reduce the social impact of related illnesses and offer better quality of life (see Appendix B).


            CONCLUSION

            HBO therapy suffers from a legacy of unqualified, non-evidence based use in the past, compounded by a lack of knowledge and teaching on the subject and paucity of hyperbaric facilities. The past decade has seen a dramatic increase in understanding of the pharmacological effects of oxygen administered in hyperbaric dosages.

            In acute surgical disorders, HBO reduces morbidity and mortality. Treatments are few in number (7-12) with obvious and significant benefits: Fewer complications, fewer new surgical procedures, better functional outcomes and reduced hospital stay. In chronic refractory disorders, therapeutic options are limited and expensive. The value of HBO lies in improving their efficacy.

            HBO therapy, when applied ethically, properly and safely by a qualified hyperbaric physician, is a powerful and valuable adjunct, and surgeons should be aware of its capability and potential to assist them in their practice.

            REFERENCES

            1. Van Zyl JJW. Gasgangreen, die moderne terapeutiese benadering. SAJS 1973;11(4):181-185.
            2. Government Gazette No 2006; 7 May 1999; Schedule 1; Prescribed Minimum Benefits; Medical Schemes Act; Section 21(1)(o).
            3. Walen R, Salzman H, Holloway D, et al. Cardiovascular and blood gas responses to hyperbaric oxygenation. Am J Cardiol 1965;15:638‑46.
            4. Krogh A: The number and distribution of capillaries in muscle with calculations of the oxygen pressure head necessary for supplying the tissue. J Physiol 1919;52:409 ‑ 415.
            5. Boerema I, Meijne NG, Brummelkamp WH, et al: Life without blood: A study of the influence of high atmospheric pressure and hypothermia on dilution of blood. J Cardiovasc Surg 1960;1:133 ‑ 146.
            6. Hunt TK, Twomey P, Zederfeldt B, et al: Respiratory gas tension and pH in healing wounds. Am J Surg 1967;1 14:302‑ 308.
            7. Sheffield PJ. Tissue oxygen measurement. In: Davis JC, Hunt TK (eds). Problem wounds, the role of oxygen. 1988. p 17 ‑ 51. Elsevier, New York.
            8. Weiss LD, Van Meter KW: The applications of hyperbaric oxygen therapy in emergency medicine. American Journal of Emergency Medicine 1992;10(6):558‑568.
            9. Zamboni WA, Roth AC, Russell RC, Graham B, Suchy H, Kucan JO. Morphological analysis of the microcirculation during reperfusion of ischemic skeletal muscle and the effect of hyperbaric oxygen. Plast Reconstr Surg 1993;91: 1110‑23.
            10. Nylander G, Lewis D, Nordstrom H, Larsson NJ. Reduction of post‑ischemic edema with hyperbaric oxygen. Plast Reconstr Surg 1985;77:596-603.
            11. Ketchum SA III, Thomas AN, Hall AD: Angiographic studies of the effects of hyperbaric oxygen on burn wound revascularization, in Wada J, Iwa T (eds): Proceedings of the Fourth International Congress in Hyperbaric Medicine. Baltimore, Williams and Wilkins, 1969, pp 388‑ 394.
            12. Marx RE: A new concept in treatment of osteoradionecrosis. Journal of Oral Maxillofacial Surgery 1983;41:351‑357.
            13. Hammarlund C, Sundberg T: Hyperbaric oxygen reduced size of chronic leg ulcers: a randomized double‑blind study. Plastic and Reconstructive Surgery 1994;93(4):829‑834.
            14. Knighton DR, Oredsson S, Banda M, et al : Regulation of repair: Hypoxic control of macrophage mediated angiogenesis, in Hunt TK, Heppenstall RB, Pines E, et al (eds): Soft and Hard Tissue Repair. New York: Praeger, 1984, pp 41‑49.
            15. Hunt TK et al. (1978) Anaerobic metabolism and wound healing ‑ an hypothesis for the initiation and cessation of collagen synthesis in wounds. Am J Surg 135:328 ‑ 332.
            16. Niniikoski J, Hunt TK: Oxygen and healing wounds: tissue‑bone repair enhancement. Handbook on Hyperbaric Medicine 1996;485‑507.
            17. Rabkin JM, Hunt TK (1988) Infection and oxygen, In: Davis JC, Hunt TK (eds) Problem wounds, the role of oxygen. Elsevier, New York 1‑16
            18. Knighton DR, Halliday B, Hunt TK: Oxygen as an antibiotic: A comparison of the effects of inspired oxygen concentration and antibiotic administration on in vivo bacterial clearance. Arch Surg 1986;121:191 ‑ 195.
            19. Marzella L, Vezzani G. Effect of hyperbaric oxygen on activity of antibacterial agents. Oriani G, Marroni A, Wattel F (Eds). Handbook of Hyperbaric Medicine; 1996; Springer, London; ISBN 3-540-75016-9.
            20. Hunt TK, Pai MP: The effect of varying ambient oxygen tensions on wound metabolism and collagen synthesis. Surg Gynecol Obstet 1972;135:561‑ 567.
            21. Thom SR, Mendiguren I, Hardy K, Bolotin T, Fisher D, Nebolon M, Kilpatrick L. Inhibition of human neutrophil beta2‑integrin‑dependent adherence by hyperbaric O2. Am J Physiol 1997;273:C770‑7.
            22. Mally R, Kolodny S. Osteogenesis enhancement. In: Hyperbaric oxygen therapy. Davis JC, Hunt TK eds, 1977. Undersea Medical Society, Bethesda MD, pp 281-285.
            23. Basset CAL, Hertzman I. Influence of oxygen concentration and mechanical factors on differentiation of connective tissue in vitro. Nature; 1967;190: 460-461.
            24. Moon RE: Treatment of gas bubble disease. Problems in Respiratory Care 1991;4(2):232‑252.
            25. Sukoff MH, Ragatz RE. Hyperbaric oxygen for the treatment of acute cerebral edema. Neurosurgery 1982; 10:29-38.
            26. Hunt TK, Niinikoski J, Zederfeldt BH. Oxygen in wound healing enhancement: cellular effects of oxygen. In: Hyperbaric oxygen therapy. Davis JC, Hunt TK eds, 1977. Undersea Medical Society, Bethesda MD, pp 111‑122.
            27. Hyperbaric Oxygen Therapy Committee Report, Hampson NH, Ed; 1999; Undersea and Hyperbaric Medical Society, Bethesda, Maryland.
            28. Hart GB, Strauss MB: Gas gangrene‑clostridial myonecrosis: a review. Journal of Hyperbaric Medicine 1990;5(2):125‑144.
            1. 29. Bakker DJ: Clostridial myonecrosis. In: Problem Wounds, The Role of Oxygen, Eds. Davis JC and Hunt TK 1988:153‑172. Elsevier Publishing Company, New York.
            30. 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;41:333‑9.
            31. Hauser CJ, Shoemaker WC. Use of transcutaneous oximetry regional perfusion index to quantify tissue perfusion in peripheral vascular disease. Ann Surg 1983; 197:337-343.
            32. Wattel F, Mattieu D, Coget JM, Billard V. Hyperbaric oxygen therapy in chronic vascular wound management. Angiology 1990; 42:59-65.
            33. Pecoraro RE, Ahroni JH, Boyko EJ, Stensel VL. Chronology and determinants of tissue repair in diabetic lower extremity ulcers. Diabetes 1991;40:1305-1313.
            34. Oriani G, Meazza D, Favales F, et
            al.: Hyperbaric oxygen therapy in diabetic gangrene. Journal of Hyperbaric Medicine 1990;5(3):171‑175.
            35. Cianci P, Petrone G, Drager S, et
            al.: Salvage of the problem wound and potential amputation with wound care and adjunctive hyperbaric oxygen therapy: an economic analysis. Journal of Hyperbaric Medicine 1988;3(3):127‑141.
            36. Doctor N, Pandya S, Supe A: Hyperbaric oxygen therapy in diabetic foot. Journal Postgrad Medicine 1992;38(3):112‑114.
            37. Faglia E, Favales F, Aldeghi A, Calia P, Quarantiello A, Oriani G, Michael M, Campagnoli P, Morabito A. Adjunctive systemic hyperbaric oxygen therapy in the treatment severe prevalently ischemic diabetic foot ulcer. A randomized study. Diabetes Care 1996;19:1338‑43.
            38. Mathieu D, Wattel F et al. (1990) Hyperbaric oxygen in the treatment of the diabetic foot. Undersea Biomed Res 17 (Suppl) :160‑161.
            39. Mathieu D, Wattle F et al. (1991) Hyperbaric oxygen in the treatment of diabetic foot lesions. J Hyperb Med 6 : 263‑ 268
            40. Knighton DR, Halliday B, Hunt TK: Oxygen as an antibiotic: A comparison of the effects of inspired oxygen concentration and antibiotic administration on in vivo bacterial clearance. Arch Surg 1986;121:191 ‑ 195.
            41. Riseman JA, Zamboni WA, Curtis A, et
            al.: Hyperbaric oxygen therapy for necrotizing fasciitis reduces mortality and the need for debridements. Surgery 1990;108:847‑850.
            42. Hollabaugh RS Jr, Fournier's Gangrene: Therapeutic Impact of Hyperbaric Oxygen. CE Plast Reconstr Surg 1998. Jan;101(1):94‑100.
            43. Cierny G, Mader JT, Pennick JJ. A clinical staging system for adult osteomyelitis. Contemp Orthop 1985; 10:17-37.
            44. Mader JT, Adams KR, Wallace WR, Calhoun JH. Hyperbaric oxygen as an adjunctive therapy for osteomyelitis. Infect Dis Clin North Am 1990; 4:433-440.
            45. Davis JC: Refractory osteomyelitis. In: Problem Wounds, The Role of Oxygen, Eds. Davis JC and Hunt TK 1988:125-142. Elsevier Publishing Company, New York.
            46. 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;142:915‑22.
            47. Marx RE, Ehler WJ, Tayapongsak P, et
            al.: Relationship of oxygen dose to angiogenesis induction in irradiated tissue. The American Journal of Surgery 1990;160:519‑524.
            48. Marx RE, Johnson RD, Kline SN: Prevention of osteoradionecrosis: A randomized prospective clinical trial of hyperbaric oxygen versus penicillin. J Am Dent Assoc 1985;III:49‑ 54.
            49. Abratt RP, Mills EE. The use of hyperbaric oxygen as an adjunct in the treatment of radionecrosis. SAMJ 1978; 54:697-699.
            50. Kindwall EP: Hyperbaric oxygen’s effect on radiation necrosis. Clinics in Plastic Surgery 1993;20(3)473‑483.
            51. Bevers RFM, Bakker DJ, Kurth KH: Hyperbaric oxygen treatment for haemorrhagic radiation cystitis. The Lancet September 23, 1995; Vol. 346: 803-805
            52. Hohenberger K. Dose‑dependent hyperbaric oxygen stimulation of human fibroblast proliferation. Wound Repair Reg 1997;5:147‑150.
            53. Zamboni WA, Roth AC, Russell RC, et
            al.: The effect of acute hyperbaric oxygen therapy on axial pattern skin flap survival when administered during and after total ischemia. Journal of Reconstructive Microsurgery 1989;5(4):343‑345.
            54. Zamboni WA, Roth AC, Russell RC, et
            al.: Morphologic analysis of the microcirculation during reperfusion of ischemic skeletal muscle and the effect of hyperbaric oxygen. Plastic and Reconstructive Surgery 1993;89(5):916‑923.
            55. Zamboni WA. Applications of hyperbaric oxygen therapy in plastic surgery. Oriani G, Marroni A, Wattel F (Eds). Handbook of Hyperbaric Medicine; 1996; 443-483. Springer, London; ISBN 3-540-75016-9.
            56. Nizgoda JAThe Effect of Hyperbaric Oxygen therapy on a burn Wound Model in Human Volunteers. Plast Reconstr Surg 1997 May;99(6):1620‑162. Double Blind. Prospective Randomised.
            1. 57. Cianci P, Lueders, HW, Lee HW, Lee H, et
            al.: Hyperbaric oxygen therapy reduces length of hospitalization in thermal burns. Journal of Burn Care and Rehabilitation 1989;10:432‑435.
            58. Cianci P, Williams C, Lueders H, et
            al.: Adjunctive hyperbaric oxygen in the treatment of thermal burns: an economic analysis. The Journal of Burn Care & Rehabilitation 1990;11(2):140‑143.
            59. Germonpre P, Reper P, Vanderkelen A: Hyperbaric oxygen therapy and piracetam decrease the early extension of deep partial‑thickness burns. Burns 1996;22(6):468‑473.
            60. Cianci P, Sato R: Adjunctive hyperbaric oxygen therapy in the treatment of thermal burns: a review. Burns 1994;20(1):5‑14.
            61. Lampl L, Frey G, Dietze T, Trausehel M. Hyperbaric oxygen in intracranial abscesses . J Hyperbaric Med 1989; 4:111 -126.
            62. Hart GB, Strauss MB. Central nervous system oxygen toxicity in a clinical setting. In: Bove AA, Bachrach AJ, Greenbaum LJ, eds. Undersea and hyperbaric physiology IX. Proceedings of the ninth international symposium on underwater and hyperbaric physiology. Bethesda, MD: Undersea and Hyperbaric Medical Society, 1987:695-699.

            Vascular and Hyperbaric Unit, Eugene Marais Hospital, Pretoria, South Africa (012) 335 8651