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  • Center for hyperbaric oxygen therapy (HBOT) and diving medicine

Hyperbaric oxygen therapy is successfully supplied to both acute as well as chronic diseases which benefit from an elevated oxygen intake.

Excellent results have been achieved for the indications recommended by the GTÜM (German society for diving and hyperbaric medicine  – Gesellschaft für Tauch- und Überdruckmedizin) and the  EUBS (European Underwater and Baromedical Society).

Hint: The english translations of the indication explanations will follow soon.

Emergency indications

  • Diving accident / compressed air accident (decompression illnesses)

    Decompression sickness (DCS) is the result of symptomatic release of gas bubbles during or after decompression after a dive. This results from tissues being oversaturated with nitrogen due to the higher pressure at greater depths: the gas bubbles can cause many symptoms. According to the latest data, in the case of professional divers and caisson workers these symptoms also include neurological manifestation as one of the most frequent symptoms. Similarly there are also frequent reports of pain around joints and in the extremities as well as non-specific symptoms. Less frequent symptoms include the skin, the inner ear and the cardiopulmonary system.

    Severe neurological manifestation can affect the central nervous system, including the brain (central manifestation) and the spine (spinal manifestation), but can also be present in the peripheral nervous system. Central manifestation covers a range of very diverse symptoms depending upon the region affected. In the case of spinal manifestations, and depending upon severity, this can also take the form of numbness, sensitive disturbances below the level of the affected spine, paralysis, bladder and colon disorders as well as pathological reflexes. Manifestations in the area of the peripheral nervous system can include for example paralyses as above, numbness and pain in the area affected or in several peripheral nerves.

    Should symptoms occur after a dive or relating to a diving accident, symptoms which indicate decompression sickness, it is vital that patients are administered pure oxygen to breathe as quickly as possible and should seek the advice of a doctor with experience in diving medicine. The medical practitioner must then decide quickly on a case-by-case basis whether the indication for the patient is for hyperbaric oxygen therapy. HBO achieves its effect on decompression sickness via a variety of mechanisms. On the one hand by way of recompression, which again reduces the volume of the nitrogen bubbles forming in the tissue. However, the main effect of HBO is the physical phenomenon referred to as the “oxygen window” which results in rapid reduction and ultimately the complete disappearance of nitrogen bubbles in human tissue.

    Therapy profile of diving accidents, US-Navy Tab. 6

    Therapy profile of diving accidents, US-Navy Tab. 6

  • Carbon monoxide poisoning, flue gas poisoning

    Carbon monoxide (CO) is a colourless, tasteless and odourless gas which results from the incomplete combustion of carbon based materials. Poisoning can occur for example in the course of domestic fires, by poorly adjusted fuel-burning heating systems or by breathing car exhaust gases in enclosed spaces.

    The symptoms caused can differ greatly from patient to patient and depend in particular on the duration of exposure and the CO concentration to which the patient is subjected. The spectrum of symptoms ranges from headache and fatigue over dizziness and confusion through to loss of consciousness as well as heart attacks (myocardial infarction) and strokes. The worst case of a severe CO intoxication is death.

    The damaging effect of CO is caused by three physiological properties:

    • As a competing oxygen antagonist having 200- to 300-times the affinity to haemoglobin (protein) compared with oxygen.
    • By binding to the myoglobin (an important oxygen carrier in muscles) and having a 30 – 40-times higher affinity for muscles.
    • By blocking the intracellular enzyme systems (e.g. cytochrome 3-oxydase) and disrupting cellular metabolism.

    The lack of cellular oxygen and the various inflammatory processes caused by CO result in tissue damage. [1]

    A patient with CO intoxication requires rapid administration of pure oxygen, there should also be a speedy and precise cardiological and neurological examination. In serious cases intensive medical care is obligatory.

    Early commencement of hyperbaric oxygen therapy can quickly and significantly elevate the proportion of oxygen bound in the blood plasma. Furthermore, the high partial oxygen pressure means, following the law of mass action, that not only is CO rapidly extracted from its bond to the haemoglobin, but it is also eliminated from its bond with the myoglobin.[2]

    It has been demonstrated that speedy commencement of hyperbaric oxygen therapy results in significant avoidance/minimisation of in particular neurological follow-up damage.  [3]

    1. Weaver, L.K., Clinical practice. Carbon monoxide poisoning. N Engl J Med, 2009. 360(12): p. 1217-25.
    2. Tirpitz, D., Aktuelle Therapie der akuten Rauchgas- und CO-Intoxikation. Prakt. Arb.med., 2009. 14: p. 8.
    3. Weaver, L.K., et al., Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med, 2002. 347(14): p. 1057-67.
  • Air and gas embolisms

    Hyperbaric oxygen therapy was originally developed as a therapy for divers suffering from nitrogen bubbles in their tissues and in their blood after too rapid decompression (surfacing).

    The ongoing further development of medical sciences, in particular in the area of interventional techniques, means that today, HBO is increasingly used to treat the accidental occurrence of air bubbles in the blood and in tissues after medical interventions. [1-10]

    The consequences of the air bubbles are reduced supply of oxygen to the tissue behind the gas bubbles, as the bubbles prevent the passage of blood-carrying oxygen to the tissue. A frequent complication in the case of arterial gas emboli is neurological damage, because the gas bubbles frequently collect in sensitive brain tissue.

    In this case patients must be given immediate hyperbaric oxygen therapy. The HBO results in rapid shrinkage of the gas bubbles in the tissue, because the elevated availability of oxygen means the nitrogen in the gas bubbles is quickly diffused back into the blood and can be breathed out. In addition, compression has the effect of reducing the volume of the gas bubbles.

    Many scientific studies report that the consequences of an arterial gas embolism with speedy administration of hyperbaric oxygen therapy results in significantly less severe neurological damage. [11-22]

    1. Lattin, G., Jr., et al., Massive systemic air embolism treated with hyperbaric oxygen therapy following CT-guided transthoracic needle biopsy of a pulmonary nodule. J Vasc Interv Radiol, 2006. 17(8): p. 1355-8.
    2. Ledowski, T., et al., Possible air embolism during eye surgery. Anesth Analg, 2005. 100(6): p. 1651-2.
    3. Tsou, M.Y., et al., Fatal gas embolism during transurethral incision of the bladder neck under spinal anesthesia. Anesth Analg, 2003. 97(6): p. 1833-4.
    4. Imasogie, N., et al., Probable gas embolism during operative hysteroscopy caused by products of combustion. Can J Anaesth, 2002. 49(10): p. 1044-7.
    5. Helmberger, T.K., U. Roth, and K. Empen, Massive air embolism during interventional laser therapy of the liver: successful resuscitation without chest compression. Cardiovasc Intervent Radiol, 2002. 25(4): p. 335-6.
    6. Raju, G.S., et al., Cerebrovascular accident during endoscopy: consider cerebral air embolism, a rapidly reversible event with hyperbaric oxygen therapy. Gastrointest Endosc, 1998. 47(1): p. 70-3.
    7. Mullins, M.E. and J.T. Beltran, Acute cerebral gas embolism from hydrogen peroxide ingestion successfully treated with hyperbaric oxygen. J Toxicol Clin Toxicol, 1998. 36(3): p. 253-6.
    8. Khan, M., et al., Coronary air embolism: incidence, severity, and suggested approaches to treatment. Cathet Cardiovasc Diagn, 1995. 36(4): p. 313-8.
    9. Abernathy, C.M. and T.C. Dickinson, Massive air emboli from intravenous infusion pump: etiology and prevention. Am J Surg, 1979. 137(2): p. 274-5.
    10. Baskin, S.E. and R.F. Wozniak, Hyperbaric oxygenation in the treatment of hemodialysis-associated air embolism. N Engl J Med, 1975. 293(4): p. 184-5.
    11. van Hulst, R.A., J. Klein, and B. Lachmann, Gas embolism: pathophysiology and treatment. Clin Physiol Funct Imaging, 2003. 23(5): p. 237-46.
    12. Benson, J., C. Adkinson, and R. Collier, Hyperbaric oxygen therapy of iatrogenic cerebral arterial gas embolism. Undersea Hyperb Med, 2003. 30(2): p. 117-26.
    13. Clarke, D., W. Gerard, and T. Norris, Pulmonary barotrauma-induced cerebral arterial gas embolism with spontaneous recovery: commentary on the rationale for therapeutic compression. Aviat Space Environ Med, 2002. 73(2): p. 139-46.
    14. Blanc, P., et al., Iatrogenic cerebral air embolism: importance of an early hyperbaric oxygenation. Intensive Care Med, 2002. 28(5): p. 559-63.
    15. Ziser, A., et al., Hyperbaric oxygen therapy for massive arterial air embolism during cardiac operations. J Thorac Cardiovasc Surg, 1999. 117(4): p. 818-21.
    16. Moon, R.E. and P.J. Sheffield, Guidelines for treatment of decompression illness. Aviat Space Environ Med, 1997. 68(3): p. 234-43.
    17. Dexter, F. and B.J. Hindman, Recommendations for hyperbaric oxygen therapy of cerebral air embolism based on a mathematical model of bubble absorption. Anesth Analg, 1997. 84(6): p. 1203-7.
    18. Catron, P.W., et al., Cerebral air embolism treated by pressure and hyperbaric oxygen. Neurology, 1991. 41(2 ( Pt 1)): p. 314-5.
    19. Leitch, D.R. and R.D. Green, Pulmonary barotrauma in divers and the treatment of cerebral arterial gas embolism. Aviat Space Environ Med, 1986. 57(10 Pt 1): p. 931-8.
    20. Mader, J.T. and W.H. Hulet, Delayed hyperbaric treatment of cerebral air embolism: report of a case. Arch Neurol, 1979. 36(8): p. 504-5.
    21. Hart, G.B., Treatment of decompression illness and air embolism with hyperbaric oxygen. Aerosp Med, 1974. 45(10): p. 1190-3.
    22. Takita, H., et al., Hyperbaric treatment of cerebral air embolism as a result of open-heart surgery. Report of a case. J Thorac Cardiovasc Surg, 1968. 55(5): p. 682-5.
  • Gas gangrene and other necrotising soft tissue infections

    Gas gangrene is a life threatening infection of soft tissues with bacteria from the Clostridium group (usually Clostridium perfringens). This can affect not only the skin and muscles, but also the lungs, the intestines and other body systems. Clostridia are strictly anaerobic bacteria, are ubiquitous and can form spores capable of surviving even the most extreme conditions.

    Gas gangrene germs produce at least twelve different toxins which act as enzymes and degrade tissue and result in cell death (necrosis) in the affected muscles.

    If therapy is not commenced within a matter of hours the risk of death is extremely high in the case of wound infections, referred to as “Clostridium myonecrosis”. Treatment includes not only antibiotics but also surgical cleaning of the wound itself. In addition, patients should also be treated with hyperbaric oxygen in order to prevent further spreading of the strictly anaerobic germ. [1-5]

    1. Glover, J.L. and J. Mendelson, Effects of Hyperbaric Oxygenation on Rabbits with Clostridium Perfringens Infection. J Trauma, 1964. 4: p. 642-51.
    2. Stevens, D.L., et al., Evaluation of therapy with hyperbaric oxygen for experimental infection with Clostridium perfringens. Clin Infect Dis, 1993. 17(2): p. 231-7.
    3. Gibson, A. and F.M. Davis, Hyperbaric oxygen therapy in the management of Clostridium perfringens infections. N Z Med J, 1986. 99(808): p. 617-20.
    4. Eltorai, I.M., et al., The role of hyperbaric oxygen in the management of Fournier’s gangrene. Int Surg, 1986. 71(1): p. 53-8.
    5. Demello, F.J., J.J. Haglin, and C.R. Hitchcock, Comparative study of experimental Clostridium perfringens infection in dogs treated with antibiotics, surgery, and hyperbaric oxygen. Surgery, 1973. 73(6): p. 936-41.

Inner ear diseases / acute inner ear perception disorders / ENT

  • Acute sudden deafness

    In the case of acute sudden deafness, there is a sudden and usually unilateral deafness for no apparent reason. The loss of hearing can vary greatly in its severity and may affect just a few frequencies or even all frequencies. This problem affects men and women equally, whereby this most frequently occurs between the ages of 43 and 53. It is often accompanied by vestibulary symptoms (e.g. dizziness). Patients with only a minor, less severe loss of hearing have excellent prospects of completely regaining their sense of hearing.[1]

    The cause of such acute sudden deafness is as yet not fully clarified. It is thought to result from the interaction of various factors which together alter the circulatory conditions within the inner ear. The use of HBO therapy in intended to ensure blood supplies (via diffusion in a healthy ear) to the hair cells even under the altered circulatory conditions.

    In a major review (Cochrane Review), it was demonstrated that HBO therapy can significantly improve hearing after an acute sudden deafness attack. [2]

    This is especially the case for younger patients (less than 50 years) [3] and patients with medium to severe loss of hearing [4]. Wherever possible HBO therapy should be administered within the first 2 weeks after the acute deafness and by latest within the first three months [4].

    1. Rauch, S.D., Clinical practice. Idiopathic sudden sensorineural hearing loss. N Engl J Med, 2008. 359(8): p. 833-40.
    2. Bennett, M.H., et al., Hyperbaric oxygen for idiopathic sudden sensorineural hearing loss and tinnitus. Cochrane Database Syst Rev, 2012. 10: p. CD004739.
    3. Topuz, E., et al., Should hyperbaric oxygen be added to treatment in idiopathic sudden sensorineural hearing loss? Eur Arch Otorhinolaryngol, 2004. 261(7): p. 393-6.
    4. Stachler, R.J., et al., Clinical practice guideline: sudden hearing loss. Otolaryngol Head Neck Surg, 2012. 146(3 Suppl): p. S1-35.
  • Acoustic trauma, noise trauma (acute noise damage)

    Hearing damage caused by noise can be divided into various subgroups:

    Depending upon the intensity and duration of the damaging acoustic waves one differentiates between acoustic trauma, blast trauma, explosion trauma and acute noise trauma.

    The sound pressure results in the loss of cells at the interface between the acoustic mechanical vibrations and the nerve signals in the cochlea in the inner ear (the corti organ), to damage to the outer hair cells, the support cells and also damage to many other anatomic structures [1]. If one measures the partial oxygen pressure in the lymphs between the skin and the bony labyrinth of the inner ear (perilymph), one can measure a significant drop in pressure [2]. Lack of oxygen in the cochlea prevents the functional metabolism of the cells, such that there is a loss of hearing.

    By increasing the partial oxygen pressure in the cochlea, in particular in the area of the peri and endo lymphs, it is possible to influence hearing cells with a metabolic disorder. However, since these cells have no vessels supplying blood but only receive oxygen by way of diffusion, an oxygen deficiency situation can only be compensated in principle by raising the ambient oxygen partial pressure.

    Moreover, hyperbaric oxygen therapy can, in the case of acute noise trauma, have a positive effect on the formation of oedema in the damaged inner ear. The clinical relevance of these processes is verified in a number of treatment studies [3-13].

    An important point to note is that an acute loss of hearing caused by noise trauma remedies itself spontaneously in around half of all cases. These spontaneous remissions usually take place within the first 48 hours after the impact of the noise. If after that time there has been no significant improvement in the symptoms, hyperbaric oxygen therapy is indicated, since after that time spontaneous remission only takes place very rarely.

    1. Morest, D.K. and B.A. Bohne, Noise-induced degeneration in the brain and representation of inner and outer hair cells. Hear Res, 1983. 9(2): p. 145-51.
    2. Lamm, K., et al., [Simultaneous determination of oxygen partial pressure in the scala tympani, electrocochleography and blood pressure values in the guinea pig]. HNO, 1989. 37(2): p. 48-55.
    3. Demaertelaere, L. and M. Van Opstal, [Treatment of acoustic trauma with hyperbaric oxygen]. Acta Otorhinolaryngol Belg, 1981. 35(3-4): p. 303-14.
    4. Pilgramm, M. and K. Schumann, Hyperbaric oxygen therapy for acute acoustic trauma. Arch Otorhinolaryngol, 1985. 241(3): p. 247-57.
    5. Pilgramm, M., Clinical and animal experiment studies to optimise the therapy for acute acoustic trauma. Scand Audiol Suppl, 1991. 34: p. 103-22.
    6. Kuokkanen, J., et al., Effect of hyperbaric oxygen treatment on permanent threshold shift in acoustic trauma among rats. Acta Otolaryngol Suppl, 1997. 529: p. 80-2.
    7. Lamm, K., H. Lamm, and W. Arnold, Effect of hyperbaric oxygen therapy in comparison to conventional or placebo therapy or no treatment in idiopathic sudden hearing loss, acoustic trauma, noise-induced hearing loss and tinnitus. A literature survey. Adv Otorhinolaryngol, 1998. 54: p. 86-99.
    8. d’Aldin, C., et al., Treatment of acoustic trauma. Ann N Y Acad Sci, 1999. 884: p. 328-44.
    9. Kuokkanen, J., A.A. Aarnisalo, and J. Ylikoski, Efficiency of hyperbaric oxygen therapy in experimental acute acoustic trauma from firearms. Acta Otolaryngol Suppl, 2000. 543: p. 132-4.
    10. Winiarski, M., et al., [Effectiveness of pharmacologic therapy combined with hyperbaric oxygen in sensorineural hearing loss following acute acoustic trauma. Preliminary report]. Pol Merkur Lekarski, 2005. 19(111): p. 348-50.
    11. Ylikoski, J., et al., Hyperbaric oxygen therapy seems to enhance recovery from acute acoustic trauma. Acta Otolaryngol, 2008. 128(10): p. 1110-5.
    12. Lafere, P., D. Vanhoutte, and P. Germonpre, Hyperbaric oxygen therapy for acute noise-induced hearing loss: evaluation of different treatment regimens. Diving Hyperb Med, 2010. 40(2): p. 63-7.
    13. van der Veen, E.L., R.A. van Hulst, and J.A. de Ru, Hyperbaric Oxygen Therapy in Acute Acoustic Trauma: A Rapid Systematic Review. Otolaryngol Head Neck Surg, 2014.
  • Outer ear infection (otitis externa maligna)

    Otitis externa necroticans is a disease much feared because it is often accompanied by serious complications and may result in death. It is an invasive inflammation of the outer ear which can result in massive loss of cells which can further spread to the skull bones and brain cells/cranial nerves. It usually affects patients with poor immune systems, e.g. diabetics in old age. They then suffer severe pain, suppuration from the outer ear, cranial nerve disorders and a significant deterioration of their general condition.

    It is vital that otititis externa receives rapid and decisive therapy. The treatment concept deserving the highest priority is not only surgical infectious source control and combined antibiotic therapy together with hyperbaric oxygenation.

    1. Shupak, A., et al., Hyperbaric oxygenation for necrotizing (malignant) otitis externa. Arch Otolaryngol Head Neck Surg, 1989. 115(12): p. 1470-5.
    2. Davis, J.C., et al., Adjuvant hyperbaric oxygen in malignant external otitis. Arch Otolaryngol Head Neck Surg, 1992. 118(1): p. 89-93.
    3. Tisch, M., et al., [The treatment of necrotizing otitis externa with a combination of surgery, antibiotics, specific immunoglobulins and hyperbaric oxygen therapy. Results of the Ulm Treatment Concept]. HNO, 2003. 51(4): p. 315-20.
    4. Narozny, W., et al., Value of hyperbaric oxygen in bacterial and fungal malignant external otitis treatment. Eur Arch Otorhinolaryngol, 2006. 263(7): p. 680-4.
    5. Ling, S.S. and C. Sader, Fungal malignant otitis externa treated with hyperbaric oxygen. Int J Infect Dis, 2008. 12(5): p. 550-2.
    6. Heiden, C., Malignant otitis externa: experience with hyperbaric oxygen therapy. Diving Hyperb Med, 2010. 40(4): p. 182.
    7. Saxby, A., et al., Malignant otitis externa: experience with hyperbaric oxygen therapy. Diving Hyperb Med, 2010. 40(4): p. 195-200.

Wound healing / problem wounds / soft tissue

  • Diabetic foot ulcers, diabetic problem wounds

    One estimate states that approximately 4 million people in Germany, i.e. around 5 % of the population, suffer from diabetes mellitus. Diabetes can result in many often severe follow-up illnesses, one of which is diabetic foot syndrome.

    Diabetic foot syndrome results from what is usually a simple trauma, in turn frequently not perceived as painful because the perception of pain is reduced due to diabetic polyneuropathy (i.e. nerve damage caused by diabetes). The consequence of this is a small wound which, because of the poor supply of oxygen due to diabetic macroangiopathy (i.e. blood circulation disorder caused by diabetes) does not heal adequately. This then leads to a large spreading ulcerisation (lesion) which then often becomes bacterially colonised and infected. This again can prevent healing of the wound. In its advanced state the worst outcome is the need to amputate the affected extremity in order to prevent sepsis (popularly known as blood poisoning) which has an extremely high mortality rate.

    Therapies include strict control of blood sugar levels, professional surgical wound treatment together with antibiotics, complemented by hyperbaric oxygen therapy: these are key therapy measures in dealing with diabetic foot syndrome. HBO has the effect of significantly improving the oxygen content of the tissue, which boosts vascular growth and has an antibacterial effect. In practice, efficacy has been verified in a number of in part major studies [1]. Today the situation is that hyperbaric oxygen therapy represents a key pillar in therapy compliant with guidelines on chronic wounds under diabetes mellitus (AWMF guideline „local therapy of chronic wounds for patients at risk of peripheral arterial blockage illness, diabetes mellitus, chronic venous insufficiency“) and has demonstrably significantly reduced the amputation rate. [2, 3] [4, 5] [5, 6]

    1. Londahl, M., et al., Hyperbaric oxygen therapy facilitates healing of chronic foot ulcers in patients with diabetes. Diabetes Care, 2010. 33(5): p. 998-1003.
    2. Kranke, P., et al., Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev, 2004(2): p. Cd004123.
    3. Abidia, A., et al., The role of hyperbaric oxygen therapy in ischaemic diabetic lower extremity ulcers: a double-blind randomised-controlled trial. Eur J Vasc Endovasc Surg, 2003. 25(6): p. 513-8.
    4. Doctor, N., S. Pandya, and A. Supe, Hyperbaric oxygen therapy in diabetic foot. J Postgrad Med, 1992. 38(3): p. 112-4, 111.
    5. Faglia, E., et al., Change in major amputation rate in a center dedicated to diabetic foot care during the 1980s: prognostic determinants for major amputation. J Diabetes Complications, 1998. 12(2): p. 96-102.
    6. Kessler, L., et al., Hyperbaric oxygenation accelerates the healing rate of nonischemic chronic diabetic foot ulcers: a prospective randomized study. Diabetes Care, 2003. 26(8): p. 2378-82.
  • Chronic, non healing wounds

    In order for a wound to heal, a large number of different processes must take place in the damaged tissue in a finely tuned and regulated sequence. Dirt and infection must be effectively combated, while at the same time the inflammation processes must decrease at the right point in time such that a regeneration of the tissue can take place. One of the essential and crucial processes is that of the new sprouting of blood vessels. Having an adequate oxygen supply is essential for many of the single steps involved.

    If the natural regeneration processes are not able to proceed, and a wound does not heal after several weeks of adequate therapy, one refers to a chronic, open wound. Frequently one of the causes is a deficient supply due to blood circulation disorders. A certain degree of oxygen insufficiency in the area of a wound is normal, and the difference between the edge of the wound being well supplied with oxygen and the wound zone being undersupplied with oxygen can actually help boost the initiation of the healing process. Having an excessive level of oxygen deficiency does, however, prevent the wound healing and results in elevated wound infection rates.

    Hyperbaric oxygenation can provide a decisive boost to wound healing in such cases. A large number of research results are available which demonstrate that the temporary hyperoxygenation of poorly supplied wounds by way of hyperbaric oxygen therapy can lessen the blocking of the wound healing process and initiate a cascade of biochemical processes which contribute towards successful healing of the wound. Effects achievable by way of HBO therapy include:

    • Provision of oxygen radicals in white blood cells (leucocytes) to combat infection
    • Effective suppression of bacterial toxin formation
    • Production of factors which boost vascular growth (VEGF – Vascular Endothelial Growth Factor) and new tissue formation (PDGF – Platelet-derived Growth Factor)
    • Enhanced release of stem cells from bone marrow
    • Increased activity of enzymes (matrix metalloproteases) which play a critical role in wound healing and vascular growth

    In this sense, hyperbaric oxygen therapy represents a critical building block in achieving the right therapy to treat chronic, non-healing wounds in a modern therapy concept, prepared in an interdisciplinary fashion by experts of various disciplines.

    1. Berg, E., et al., The use of adjunctive hyperbaric oxygen in treatment of orthopedic infections and problem wounds: an overview and case reports. J Invest Surg, 1989. 2(4): p. 409-21.
    2. Hammarlund, C. and T. Sundberg, Hyperbaric oxygen reduced size of chronic leg ulcers: a randomized double-blind study. Plast Reconstr Surg, 1994. 93(4): p. 829-33; discussion 834.
    3. Otto, G.H., C. Buyukcakir, and C.E. Fife, Effects of smoking on cost and duration of hyperbaric oxygen therapy for diabetic patients with non-healing wounds. Undersea Hyperb Med, 2000. 27(2): p. 83-9.
    4. Dolezal, V., [Hyperbaric oxygen therapy in non-healing wounds and defects] ]. Cas Lek Cesk, 2001. 140(4): p. 104-7.
    5. Kranke, P., et al., Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev, 2004(2): p. Cd004123.
    6. Health Quality, O., Hyperbaric oxygen therapy for non-healing ulcers in diabetes mellitus: an evidence-based analysis. Ont Health Technol Assess Ser, 2005. 5(11): p. 1-28.
    7. Korpinar, S., et al., Adjunctive hyperbaric oxygen therapy in radiation-induced non-healing wound. J Dermatol, 2006. 33(7): p. 496-7.
    8. Oubre, C.M., et al., Retrospective study of factors affecting non-healing of wounds during hyperbaric oxygen therapy. J Wound Care, 2007. 16(6): p. 245-50.
    9. Kulikovsky, M., et al., Hyperbaric oxygen therapy for non-healing wounds. Isr Med Assoc J, 2009. 11(8): p. 480-5.
    10. Melamed, Y. and H. Bitterman, Non-healing wounds and hyperbaric oxygen: a growing awareness. Isr Med Assoc J, 2009. 11(8): p. 498-500.
    11. Londahl, M., et al., Hyperbaric oxygen therapy facilitates healing of chronic foot ulcers in patients with diabetes. Diabetes Care, 2010. 33(5): p. 998-1003.
    12. Feldman-Idov, Y., Y. Melamed, and L. Ore, Improvement of ischemic non-healing wounds following hyperoxygenation: the experience at Rambam-Elisha Hyperbaric Center in Israel, 1998-2007. Isr Med Assoc J, 2011. 13(9): p. 524-9.
    13. O’Reilly, D., et al., A prospective, double-blind, randomized, controlled clinical trial comparing standard wound care with adjunctive hyperbaric oxygen therapy (HBOT) to standard wound care only for the treatment of chronic, non-healing ulcers of the lower limb in patients with diabetes mellitus: a study protocol. Trials, 2011. 12: p. 69.
  • Endangered skin and/or musculo-skeletal grafts

    In general, the transplant of flap grafts and skin transplants does not require additional therapies, because modern surgical techniques achieve excellent results. However, in certain situations the healing of the transplant can be rendered more difficult. In this regard, complications are known to occur in areas subjected to medical radiation treatments, after pronounced soft tissue damage or in areas of shear injuries. In such cases the process of healing can be preventatively supported by hyperbaric oxygen therapy. When this has not occurred, and when grafts are rejected by the body, the situation can sometimes only be saved by way of hyperbaric oxygen therapy, thus avoiding the need for renewed transplantation.

    The scientific literature in this area complements practical experience by presenting a large number of animal studies [1-11], as well as clinical trials [12-14] and case series [15-19] which all verify the positive effect of HBO.

    1. Prada, F.S., et al., Effect of allopurinol, superoxide-dismutase, and hyperbaric oxygen on flap survival. Microsurgery, 2002. 22(8): p. 352-60.
    2. Agir, H., et al., [Histologic effects of hyperbaric oxygen therapy administered immediately after or two hours after ischemia-reperfusion injury: a rat abdominal skin flap model]. Kulak Burun Bogaz Ihtis Derg, 2003. 10(1): p. 18-24.
    3. Hong, J.P., et al., The effect of hyperbaric oxygen on ischemia-reperfusion injury: an experimental study in a rat musculocutaneous flap. Ann Plast Surg, 2003. 51(5): p. 478-87.
    4. Richards, L., et al., Effect of hyperbaric oxygen therapy on the tubed pedicle flap survival in a rat model. Ann Plast Surg, 2003. 50(1): p. 51-6.
    5. Zhang, T., et al., Efficacy of hyperbaric oxygen on survival of random pattern skin flap in diabetic rats. Undersea Hyperb Med, 2007. 34(5): p. 335-9.
    6. Selcuk, C.T., et al., The effect of hyperbaric oxygen therapy on the survival of random pattern skin flaps in nicotine-treated rats. J Plast Reconstr Aesthet Surg, 2012. 65(4): p. 489-93.
    7. Baynosa, R.C., et al., The effect of hyperbaric oxygen on nitric oxide synthase activity and expression in ischemia-reperfusion injury. J Surg Res, 2013. 183(1): p. 355-61.
    8. Demirtas, A., et al., Effect of hyperbaric oxygen therapy on healing in an experimental model of degloving injury in tails of nicotine-treated rats. J Hand Surg Eur Vol, 2013. 38(4): p. 405-11.
    9. Liang, F., et al., Effect of HMGB1/NF-kappaB in hyperbaric oxygen treatment on decreasing injury caused by skin flap grafts in rats. Eur Rev Med Pharmacol Sci, 2013. 17(15): p. 2010-8.
    10. Qi, Z., et al., Effects of hyperbaric oxygen preconditioning on ischemia-reperfusion inflammation and skin flap survival. Chin Med J (Engl), 2013. 126(20): p. 3904-9.
    11. Kang, N., et al., Preconditioned hyperbaric oxygenation protects skin flap grafts in rats against ischemia/reperfusion injury. Mol Med Rep, 2014. 9(6): p. 2124-30.
    12. Perrins, D.J., Hyperbaric oxygenation of skin flaps. Preliminary report. Br J Plast Surg, 1966. 19(2): p. 110-2.
    13. Perrins, D.J., Influence of hyperbaric oxygen on the survival of split skin grafts. Lancet, 1967. 1(7495): p. 868-71.
    14. Roje, Z., et al., Influence of adjuvant hyperbaric oxygen therapy on short-term complications during surgical reconstruction of upper and lower extremity war injuries: retrospective cohort study. Croat Med J, 2008. 49(2): p. 224-32.
    15. Mathieu, D., et al., Pedicle musculocutaneous flap transplantation: prediction of final outcome by transcutaneous oxygen measurements in hyperbaric oxygen. Plast Reconstr Surg, 1993. 91(2): p. 329-34.
    16. Saber, A.A., et al., A new approach in the management of chronic nonhealing leg ulcers. J Invest Surg, 2005. 18(6): p. 321-3.
    17. Gonnering, R.S., E.P. Kindwall, and R.W. Goldmann, Adjunct hyperbaric oxygen therapy in periorbital reconstruction. Arch Ophthalmol, 1986. 104(3): p. 439-43.
    18. Friedman, H.I., C. Stonerock, and A. Brill, Composite earlobe grafts to reconstruct the lateral nasal ala and sill. Ann Plast Surg, 2003. 50(3): p. 275-81; discussion 281.
    19. Assaad, N.N., et al., Use of adjuvant hyperbaric oxygen therapy to support limbal conjunctival graft in the management of recurrent pterygium. Cornea, 2011. 30(1): p. 7-10.
  • Wide-spread and/or deep soft tissue injury (crush injury, compartment syndrome)


    Crush injuries, i.e. injuries caused by the traumatic impact of external forces on the body, can result in damage to different types of tissue, such as muscles, nerves, blood vessels and the skin. Such injuries frequently result in wounds being slow or difficult to heal because the supply of oxygen which is so vital for the healing process is often detrimentally affected by vascular system disorders. The flow of blood in the wound area is often further prejudiced by fluids collecting in tissues (oedema formation). In cases in which such oedemas are accompanied by increased pressure in enclosed compartments (e.g. within muscle facies), one has a situation known as the compartment syndrome. This serious condition builds into a vicious circle comprising a disruption of the blood flow caused by the oedema and in turn further oedema formation and so on, which can ultimately cause serious consequential damage. If the circulation of the blood can be re-established, the toxic substances can be transported away from the tissues previously disconnected from the blood supply. These toxic substances can result in severe damage within the human body to the extent that affected patients require intensive medical care and monitoring.

    The objective is to identify the risk of the compartment syndrome at an early stage and treat it preventively.

    Hyperbaric oxygen therapy results in the narrowing of the blood vessels, effectively reducing the flow of blood to the damaged tissue by some 20 % [1, 2], and hence has the effect of decreasing the inflow while maintaining the same outflow rate, creating an anti-oedema effect. This helps reduce pressure in the tissue, which then improves the flow of blood in the smaller diameter capillaries (micro circulation). In this fashion and also because of the higher oxygen concentration in the blood plasma, the damaged tissue receives a better supply of the oxygen so vital for regeneration. Further positive effects are initiated at a cellular level.

    1. Nylander, G., et al., Reduction of postischemic edema with hyperbaric oxygen. Plast Reconstr Surg, 1985. 76(4): p. 596-603.
    2. Bird, A.D. and A.B. Telfer, Effect of Hyperbaric Oxygen on Limb Circulation. Lancet, 1965. 1(7381): p. 355-6.
    3. Garcia-Covarrubias, L., et al., Adjuvant hyperbaric oxygen therapy in the management of crush injury and traumatic ischemia: an evidence-based approach. Am Surg, 2005. 71(2): p. 144-51.
    4. Bouachour, G., et al., Hyperbaric oxygen therapy in the management of crush injuries: a randomized double-blind placebo-controlled clinical trial. J Trauma, 1996. 41(2): p. 333-9.

Bone and bone marrow diseases

  • Chronic inflammation of periosteum and bone (osteitis, osteomyelitis)

    Bacterial inflammations of bone are referred to as osteitis, inflammations of the bone marrow as osteomyelitis. The colonising bacteria may have their source either externally, after accidents or due to foreign materials introduced in the course of therapies, as well as internal, due to tracking within the body. Patients affected often suffer from general symptoms such as simply feeling ill, fever and shivering, while locally osteitis/osteomyelitis is expressed through pain and doughy soft tissue swelling.

    The therapy of acute osteitis and/or osteomyelitis requires rapid administration of antibiotics. It may be necessary to surgically clean infectious areas. Regretfully it is often the case that despite adequate therapy a chronic course may take place involving recurrent inflammation flare-ups. This is known as chronic osteitis/osteomyelitis. Although in such cases there are generally fewer general complaints, the illness is present in the form of pain and swelling/thickening of the affected bones. If allowed to advance it may cross to neighbouring joints or result in instability of the bones affected, which is a further reason why the situation should be prevented as far as possible. In particular, if it becomes apparent that the conservative therapy is no longer having an adequate effect, hyperbaric oxygen therapy is often able to make an important contribution to allowing the long-term healing process to ultimately come to a successful conclusion. This is due to a number of effects of hyperbaric oxygen therapy [1] triggered by elevating the oxygen content in the inflammatory milieu (which has a low oxygen level) [2]. Typical HBO effects are because some white blood cells, those which absorb bacteria and kill them with oxygen radicals, require a certain level of oxygen to be present in the tissue in order to exercise their function. Furthermore it may also be stated that a certain level of oxygen is necessary in the surrounding areas in order for some antibiotics to be absorbed into the colonising bacteria. That these effects are often clinically relevant has been verified for example in many animal studies [3-7] and also in the results of some clinical case studies [8-10].

    1. Park, M.K., R.A. Myers, and L. Marzella, Oxygen tensions and infections: modulation of microbial growth, activity of antimicrobial agents, and immunologic responses. Clin Infect Dis, 1992. 14(3): p. 720-40.
    2. Niinikoski, J. and T.K. Hunt, Oxygen tensions in healing bone. Surg Gynecol Obstet, 1972. 134(5): p. 746-50.
    3. Mader, J.T., et al., Therapy with hyperbaric oxygen for experimental osteomyelitis due to Staphylococcus aureus in rabbits. J Infect Dis, 1978. 138(3): p. 312-8.
    4. Triplett, R.G. and G.B. Branham, Treatment of experimental mandibular osteomyelitis with hyperbaric oxygen and antibiotics. Int J Oral Surg, 1981. 10(Suppl 1): p. 178-82.
    5. Mader JT, A.K., Couch LA, Potentiation of tobramycin by hyperbaric oxygen in experimental Pseudomonas aeruginosa osteomyelitis. 27th Interscience Concerence on Antimicrobial Agents and Chemotherapy, New York, 1987.
    6. Mendel V, e.a., Therapy with hyperbaric oxygen and cefazolin for experimental osteomyelitis due to Staphylococcus aureus in rats. Undersea Hyperb Med., 1999. 26(3): p. 169-174.
    7. Mendel V, S.H., Scholz H. , Synergy of HBO2 and a local antibiotic carrier for experimental osteomyelitis due to Staphylococcus aureus in rats. . Undersea Hyperb Med. , 2004. 31(4): p. 407-416.
    8. Barili, F., et al., Role of hyperbaric oxygen therapy in the treatment of postoperative organ/space sternal surgical site infections. World J Surg, 2007. 31(8): p. 1702-6.
    9. Roje, Z., et al., Influence of adjuvant hyperbaric oxygen therapy on short-term complications during surgical reconstruction of upper and lower extremity war injuries: retrospective cohort study. Croat Med J, 2008. 49(2): p. 224-32.
    10. Yu WK, e.a., Hyperbaric oxygen therapy as an adjunctive treatment for sternal infection and osteomyelitis after sternotomy and cardiothoracic surgery. J Cardiothorax Surg., 2011. 6:141.
  • Circulatory disorders of the bone, aseptic bone necroses (including femoral head necroses, morbus Ahlbäck)

    Patients suffering from aseptic bone necrosis typically complain of a rapid build-up of load-dependent pain in the affected region of the body without any identifiable cause.

    This is due to the sudden deterioration of the end part of a bone (epiphysis) although practically any part of the body can be affected. The symptoms for the various structures affected in this way are named after of the first observer and reporter of that particular configuration (e.g. Perthes disease, Ahlback disease, Kohler disease etc.).

    The fact that aseptic bone necroses often occur during childhood has resulted in the supposition that there is a growth-dependent discrepancy between bone growth and supplies to the bone. Furthermore other risk factors are known, such as the administration of cortisone medications.

    Hyperbaric oxygen therapy can be used as a conservative method having few side effects offering good success in aseptic bone necroses. The mode of efficacy is seen in its supportive oxygen supply and in HBO having a boosting effect on bone metabolism. In addition in the case of femoral head necrosis good clinical experience is also supported in excellent study results [12], which in this case provide impressive documentation of the efficacy of HBO.

    1. Bennett, M., Hyperbaric oxygen therapy improved both pain scores and range of motion in patients with early idiopathic femoral head necrosis (Ficat stage II). Diving Hyperb Med, 2011. 41(2): p. 105.
    2. Camporesi, E.M., et al., Hyperbaric oxygen therapy in femoral head necrosis. J Arthroplasty, 2010. 25(6 Suppl): p. 118-23.
  • Bone marrow oedema syndrome

    In the case of bone marrow oedema syndrome, the patient suffers from increased collection of water and increased pressure in the bone. This can be identified in images generated in magnetic resonance tomography. Patients affected suffer from severe, therapy-resistant pain and restricted movements in the joints affected. The typical pain pattern of BMO is a mechanical pain dependent upon mechanical load in conjunction with dull, tormenting permanent pain which is also present when at rest.

    Bone marrow oedema syndrome is differentiated into three clinical groups:

    • Ischemic bone marrow oedema is sometimes seen as a consequence of or associated illness to various bone diseases. Typical illnesses are osteonecrosis, ostochondrosis dissecans, Ahlback disease and chronic regional pain syndrome (CRPS, formerly Sudeck’s atrophy).
    • Mechanical bone marrow oedema results from contusions, micro and stress fractures and is also referred to as „bone bruises“.
    • Reactive BMO is the consequence of arthrosis or tumours.

    Specific forms of BMO are present in the femur after pregnancy while the idiopathic form has no identifiable cause.

    Causes discussed are neural (i.e. dependent upon nerves), humoral (affecting body fluids) and circulatory (i.e. to do with the blood circulation). Osteoclasts (cells vital for bone metabolism) play a decisive role, since they are able to create an acidic milieu within the bone. The exact etiology of bone marrow oedema is, however, the subject of discussion. Similarly, the exact reasons for the effect of hyperbaric oxygen therapy on bone marrow oedema are also unknown. Discussions refer to the known swelling reduction (antioedomatic) effect, the inflammation controlling effect and the bone metabolism regulating effect of HBO.

Prevention and therapy of radiation damage

  • Late radiation damage after breast cancer therapy

    Breast cancer is by far the most frequent malign disease affecting women. Statistically speaking, every eighth woman in Germany will suffer this illness during her lifetime. Luckily, research in the field of breast cancer therapy has made great advances. Treatments available include surgical therapy, chemotherapy with various substance classes as well as radiation therapy, which is for example always administered when surgery had been of the breast-conserving type. In the case of radiation therapy there are often side effects. A typical example is so-called acute radiation damage shortly after the therapy in the area impacted by the radiation appearing in the form of reddening of the skin or wet skin scaling which, however, usually both discontinue and heal without leaving any traces after a short period. Much more problematic is so-called late radiation damage which can occur in up to 10 per cent of all cases [1]. In this case cells may die even several months or years after completion of the therapy resulting in pain, swelling, tissue changes (fibrosation) and pathological changes to skin capillaries (teleangyectasesias) in the radiation field.

    Hyperbaric oxygen therapy has been used in the therapy of late radiation damage since the 1970s to great effect [2]. In the interim, the efficacy has been verified in many studies [34]. In this case it must be borne in mind that HBO represents an important building block in a multi-modal therapy concept. In particular in severe cases with pronounced necrosis (cell death), it is sometimes the case that despite the good efficacy of the HBO therapy it is nonetheless not possible to avoid concurrent surgical intervention.

    1. Weaver, L.K., Hyperbaric Oxygen Therapy Indications. Undersea and Hyperbaric Medical Society, 2014. 13th Edition.
    2. Hart, G.B. and E.G. Mainous, The treatment of radiation necrosis with hyperbaric oxygen (OHP). Cancer, 1976. 37(6): p. 2580-5.
    3. Carl, U.M., et al., Hyperbaric oxygen therapy for late sequelae in women receiving radiation after breast-conserving surgery. Int J Radiat Oncol Biol Phys, 2001. 49(4): p. 1029-31.
    4. Fink, D., et al., Hyperbaric oxygen therapy for delayed radiation injuries in gynecological cancers. Int J Gynecol Cancer, 2006. 16(2): p. 638-42.
  • Radiation cystitis after irradiation

    Following radiation of the pelvis as well as the colon, it is possible for late radiation damage to occur to the bladder. Happily this is only rarely the case, but when it does it is difficult to treat and represents a very serious symptom which in the worst case may result in death [1]. Symptoms which occur in the case of radiation cystitis are pain when urinating, blood in urine, increased frequency of urge to urinate, increased numbers of urinary tract infections and urinary incontinence. In a number of case studies various authors have reported the positive effect of hyperbaric oxygen therapy on radiation cystitis [2-5]. This is all the more noticeable when one considers the serious course of such illnesses without adequate successful therapy [1].

    1. Li, A., J. Sun, and H. Chao, [Late bladder complications following radiotherapy of carcinoma of the uterine cervix]. Zhonghua Fu Chan Ke Za Zhi, 1995. 30(12): p. 741-3.
    2. Bevers, R.F., D.J. Bakker, and K.H. Kurth, Hyperbaric oxygen treatment for haemorrhagic radiation cystitis. Lancet, 1995. 346(8978): p. 803-5.
    3. Corman, J.M., et al., Treatment of radiation induced hemorrhagic cystitis with hyperbaric oxygen. J Urol, 2003. 169(6): p. 2200-2.
    4. Chong, K.T., N.B. Hampson, and J.M. Corman, Early hyperbaric oxygen therapy improves outcome for radiation-induced hemorrhagic cystitis. Urology, 2005. 65(4): p. 649-53.
    5. Neheman, A., et al., Hyperbaric oxygen therapy for radiation-induced haemorrhagic cystitis. BJU Int, 2005. 96(1): p. 107-9.
    6. Hampson, N.B., et al., Prospective assessment of outcomes in 411 patients treated with hyperbaric oxygen for chronic radiation tissue injury. Cancer, 2012. 118(15): p. 3860-8.
  • Radiation proctitis in rectal area after irradiation

    Radiation proctitis describes the damage to the mucus membrane in the rectal area as resulting after irradiation of structures located within the pelvis (e.g. colon, uterus, bladder, prostate). Depending upon time of occurrence of proctitis, one differentiates between early and late stage.

    Early damage occurs directly after the radiation due to the high rate of cell division and the associated sensitivity of the colon mucosa to radiation. Patients suffer from painful stool, diarrhoea, flatulence as well as evacuation of blood and mucus stool. The complaints often recede within a number of weeks without leaving any permanent damage.

    Late damage arises after months or years. An increase in connecting tissue (fibroses) and vascular changes can result in a lack of oxygen in the colon mucosa with in turn consequential chronic transformation processes. The patients then suffer from the same symptoms as in the early stage. In addition it is, however, possible for the colon to narrow, which can be life threatening. Ulcerisation often occurs in the mucosa as do pathological connections between different colon sections (fistula). These complaints are often unresponsive to treatment and do not infrequently result in surgical intervention.

    In order to avoid such operations, HBO often represents a benign and low risk additional treatment method in the case of chronic radiation proctitis which is not responsive to medication, because the central cause of this disease is oxygen deficiency. HBO is able to trigger the new formation of vessels, vascular growth which has reached a level of up to 80 % of the vascular density of normal tissue (Marx 85).

    The good efficacy of HBO has been verified not only in many case descriptions and smaller studies [1, 2] [3], but also has already been given evidence degree Ib in major studies.[4]

    1. Nakada, T., et al., Successful hyperbaric oxygenation for radiation cystitis due to excessive irradiation to uterus cancer. Eur Urol, 1992. 22(4): p. 294-7.
    2. Charneau, J., et al., Severe hemorrhagic radiation proctitis advancing to gradual cessation with hyperbaric oxygen. Dig Dis Sci, 1991. 36(3): p. 373-5.
    3. Oliai, C., et al., Hyperbaric oxygen therapy for radiation-induced cystitis and proctitis. Int J Radiat Oncol Biol Phys, 2012. 84(3): p. 733-40.
    4. Clarke, R.E., et al., Hyperbaric oxygen treatment of chronic refractory radiation proctitis: a randomized and controlled double-blind crossover trial with long-term follow-up. Int J Radiat Oncol Biol Phys, 2008. 72(1): p. 134-143.

Diseases of the eye

  • Anterior ischemic optic neuropathy (central retinal artery occlusion of the eye)

    When the human eye “sees” it does so by way of the retina, which receives its blood supply centrally from the arteria centralis retinae and peripherally from the areteria ciliares. If the flow of blood through these vessels, in particular through the arteria centralis retinae, is disturbed, this is usually accompanied by a loss of sight, which can result in a permanent loss of vision.

    Hyperbaric oxygen therapy is able to keep the sensory cells alive in many cases provided the therapy is started speedily, such that the recannalisation, which in the most cases has commenced after approx. 72 hours, means the situation does not result in irreversible cell death.

    The effect of HBO has been verified in a number of case studies. [1-6]

    1. Bojic, L., et al., Hyperbaric oxygen for the treatment of nonarteritic anterior ischemic optic neuropathy. Acta Med Croatica, 1995. 49(3): p. 133-6.
    2. Arnold, A.C., et al., Hyperbaric oxygen therapy for nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol, 1996. 122(4): p. 535-41.
    3. Aisenbrey, S., et al., [Hyperbaric oxygen therapy in retinal artery occlusion]. Ophthalmologe, 2000. 97(7): p. 461-7.
    4. Weiss, J.N., Hyperbaric oxygen treatment of retinal artery occlusion. Undersea Hyperb Med, 2010. 37(3): p. 167-72.
    5. Cope, A., J.V. Eggert, and E. O’Brien, Retinal artery occlusion: visual outcome after treatment with hyperbaric oxygen. Diving Hyperb Med, 2011. 41(3): p. 135-8.
    6. Menzel-Severing, J., et al., Early hyperbaric oxygen treatment for nonarteritic central retinal artery obstruction. Am J Ophthalmol, 2012. 153(3): p. 454-459 e2.

Experimental

  • Post-contusional syndrome

    Traumatic brain injuries (head and brain trauma), e.g. as a result of traffic accidents, accidents in the home or in sport, are frequently the cause of chronic complaints and significant restrictions to activities of daily life. They can result in a massive reduction in quality of life. In the USA, head and brain injuries are the most frequent causes of death and illness (morbidity) overall [1]

    In those cases where the trauma is accompanied by loss of consciousness but also in the case of relatively mild head and brain injuries (even without loss of consciousness), there can be long-term complaints even after the acute aspects have disappeared,. These comprise a number of different and diverse symptoms, such as headache, dizziness, fatigue, irritability, lack of concentration, memory disorders, sleep disorders and reduced ability to cope with stress, emotional stimulation or alcohol [2] (ICD-10 F07.2). Other symptoms described include changes to affect (anxiety or depression), personality changes and lethargy [3] (DSM-IV criteria).

    An animal study was able to show that HBO therapy can have a positive effect on learning in rats after head brain injury [4]. However, it has also been shown in the case of humans that HBO therapy after traumatic brain injury and in the case of post-contusional syndrome has a positive effect on cognition and on the quality of life of the patient and can help in reducing symptoms by enhancing brain metabolism (in brain imaging) [5, 6] [7]

    1. Coronado, V.G., et al., Surveillance for traumatic brain injury-related deaths–United States, 1997-2007. MMWR Surveill Summ, 2011. 60(5): p. 1-32.
    2. Boake, C., et al., Diagnostic criteria for postconcussional syndrome after mild to moderate traumatic brain injury. J Neuropsychiatry Clin Neurosci, 2005. 17(3): p. 350-6.
    3. Yeates, K.O. and H.G. Taylor, Neurobehavioural outcomes of mild head injury in children and adolescents. Pediatr Rehabil, 2005. 8(1): p. 5-16.
    4. Harch, P.G., et al., Hyperbaric oxygen therapy improves spatial learning and memory in a rat model of chronic traumatic brain injury. Brain Res, 2007. 1174: p. 120-9.
    5. Boussi-Gross, R., et al., Hyperbaric oxygen therapy can improve post concussion syndrome years after mild traumatic brain injury – randomized prospective trial. PLoS One, 2013. 8(11): p. e79995.
    6. Golden, Z.L., et al., Improvement in cerebral metabolism in chronic brain injury after hyperbaric oxygen therapy. Int J Neurosci, 2002. 112(2): p. 119-31.
    7. Golden, Z., C.J. Golden, and R.A. Neubauer, Improving neuropsychological function after chronic brain injury with hyperbaric oxygen. Disabil Rehabil, 2006. 28(22): p. 1379-86.





Contact Details

Centre for hyperbaric oxygen therapy (HBOT) and diving medicine