Covered Conditions For Hyperbaric Oxygen Therapy
Brief Narrative Summary of Key Indication-Specific Literature
Prepared for the Health Care Financing Administration (Medicare)
~ Medicare
Coverage Issues Manual 35-10
Dick Clarke, CHT
Program Director, Hyperbaric Medicine Service
Palmetto Richland Memorial Hospital
Columbia, South Carolina
1. ACUTE CARBON MONOXIDE INTOXICATION
Bartlett, R: Carbon monoxide poisoning. Clinical management of poisoning and drug overdose. WB Saunders, Lester M Haddad, James F Winchester editors; 3rd edition; 1997
General review article, emphasizing both the modern appreciation of the complex pathophysiology involved, and the multifactorial benefits of HBO therapy.
Thom, SR: Carbon monoxide-mediated brain lipid peroxidation in the rat. J. Appl. Physiol. 1990;68(3): 997-1003
A publication that advanced the pathophysiology of CO poisoning from the simple concept of inhibition of hemoglobin function. This data indicates that critical cellular toxicity occurs.
Thom, SR: Antagonism of carbon monoxide-mediated brain lipid peroxidation by hyperbaric oxygen. Toxicol. Appl. Pharmacol. 1990; 105: 340-344
In reference to the above elucidation of a cellular poisoning, this companion study demonstrates the ability of HBO therapy to inhibit the toxic process.
Thom, SR: Leukocytes in carbon monoxide-mediated brain oxidative injury. Toxicol. Appl. Pharmacol. 1993; 123: 243-247
Recent evidence of complex tissue injury, here involving a leukocyte -mediated brain injury as a result of acute CO poisoning.
Thom, SR: Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon- monoxide-mediated brain injury in rats. Toxicol. Appl. Pharmacol. 1993; 123: 248-256
A companion article to that pathophysiology noted in the previous article. This research demonstrates the functional inhibition of leukocytes by HBO therapy, thereby antagonizing CO medicated oxidative brain injury. Clearly, CO poisoning involves multiple and complex pathologies. Hyperbaric oxygen has been consistently demonstrated as antagonistic to these processes: something no other intervention, including oxygen delivered without a hyperbaric chamber, has demonstrated.
Myers RAM, Snyder SK, Emhoff TA: Subacute sequelae of carbon monoxide poisoning. Ann Emerg Med. December 1985; 14: 1163-1167
A large case series that reports the ability of HBO therapy to minimize/eliminate post exposure relapse, which occurred in 12% of CO poisoned patients not treated hyperbarically. The reader is asked to consider the morbidity and cost (work-related absence, etc.) associated with such sequelae.
Norkool DM, Kirkpatrick JN: Treatment of acute carbon monoxide poisoning with hyperbaric oxygen: A review of 115 cases. Ann Emerg Med. December 1985; 14: 1168-1171
Further evidence of the significant (43%) relapse/ late complications that characterize CO poisoned patients who do not receive hyperbaric oxygenation.
Van Hoesen KB, Camporesi EM, Moon RE, Hage ML, Piantadosi CA: Should hyperbaric oxygen be used to treat the pregnant patient for acute carbon monoxide poisoning? A case report and literature review. JAMA 1989; 261: 1039-1043
A report of the heightened risk/morbidity/mortality to the fetus in maternal CO poisoning. The authors provide a recommended management protocol that centers around HBO therapy.
McNulty JA, Maher BA, Chu M, ET AL.: Relationship of short-term verbal memory to the need for hyperbaric oxygen treatment after carbon monoxide poisoning. Neuropsychiatry, Neuropsychology and Behavioral Neurology 1997;10: 174-179
A case controlled study demonstrating the benefit of HBO therapy in improving short-term memory following CO exposure.
Thom SR, Taber RL, Mendiguren II, Clark JM, Hardy KR, Fisher AB: Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Annuals of Emergency Medicine. April 1995; 25:4: 474-480
Prospective randomized clinical trial that confirms the findings of above noted and non-controlled reports: namely: HBO therapy "decreased the incidence of delayed neurological sequelae after CO poisoning."
Ducasse JL, Celsis P, Marc-Vergnes JP: Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation? Undersea Hyperbaric Med 1995; 22(1): 9-15
Prospective and randomized blinded clinical trial. The authors conclude that HBO therapy "reduces the time of initial recovery and the number of delayed functional abnormalities…"
Jiang J, Tyssebotn I: Normobaric and hyperbaric oxygen treatment of acute carbon monoxide poisoning in rats. Undersea Hyperbaric Med 1997; 24(2): 107-116
A comparative trial of various groups; involving no treatment, pressurized air treatment and pressurized oxygen treatment, in a severe CO and cerebral ischemic model. "Compared to normoxic treatments, the HBO… significantly reduced the mortality and neurologic morbidity." HBO was also significantly better than ‘normal oxygen’ in increasing survival rate…"
2. DECOMPRESSION ILLNESS (sic SICKNESS)
Note
In the context of the Medicare 35-10 document, this "Covered Condition" refers to Decompression Sickness. Modern (post-1995) terminology defines Decom-pression Illness as the syndrome of gas-induced disease that encompasses both Gas Embolism and Decompression Sickness. This evolution is, in part, the result of the frequent difficulty in distinguishing these conditions when they involve a barotraumatic etiology.
Anon: U.S. Navy Diving Manual, Volume 1 (Air Diving) 1993; Revision 3:8-22--8-28. Best Publishing Company, Flagstaff, Arizona.
The authoritative text of the United States military government. It states, among other things, that "Any decompression sickness that occurs must be treated with recompression (hyperbaric oxygen therapy)".
Anon: NOAA Diviing Manual, Diving for Science and Technology 1991;20-8--20-9.
The authoritative text of the United States civilian government. It states, among other things, "The only adequate treatment for … gas embolism in divers is recompression in a recompression (hyperbaric) chamber".
Rudge FW, Shafer, MR: The effect of delay on treatment outcome in altitude-induced decompression sickness. Aviat. Space Environ. Med. 1991;62:687-690.
A military government review of 232 cases of decompression sickness. The success of treatment was inversely related to delay in treatment. Stated differently, closure or non-availability of local and regional hyperbaric treatment facilities is likely to result in career/occupatiol ending sequelae, with the not insignificant longitudinal health costs associated with rehabilitation and supportive care.
Melamed Y, Shupak A, Bitterman H: Medical problems associated with underwater diving. The New England Journal of Medicine 1992;326(1):30-35.
A comprehensive review article. It identifies a critical diagnostic issue in that subtle neurological injury may co-exist with less severe musculoskeletal involvement. Non-diving/hyperbaric specialists may well miss this point, resulting in inappropriate treatment, and long term (and costly)morbidity.
Hallenbeck JM, Bove AA, Elliott DH: Mechanisms underlying spinal cord damage in decompression sickness. Neurology 1975;25:308-316
A fundamental determination of the evolution of decompression sickness, demonstrating obstruction and ischemia of the spinal cord venous drainage, resulting in infarction. No intervention other than hyperbaric oxygenation has been tried or proposed as therapeutically appropriate and able to reverse this process. Pharmacologic adjuncts are actively under investigation. However, the fundamental issue is reduction/elimination of gaseous emboli. Hyperbaric pressurization must, therefore, be considered mandatory.
VanDerAue OE, Duffner GJ, Behnke AR: The treatment of decompression sickness: an analysis of one hundred and thirteen cases. The Journal of Industrial Hygiene and Toxicology 1947;29(6):359-366.
An historically important paper. It describes, in a large clinical series, the effectiveness of hyperbaric therapy in the successful resolution of wide-ranging presentations, involving both the nervous and musculoskeletal systems.
Millington T: "No tech" technical diving: the lobster divers of La Mosquitia. SPUMS Journal 1997;27(3):147-148
An example of the resulting human toll when decompression sickness sufferers do not undergo hyperbaric oxygen therapy. "Inundated with paralyzed divers".
Green JW, Tichenor J, Curley MD: Treatment of type I decompression sickness using the U.S. Navy treatment algorithm. Undersea Biomed Res 1989;16(6):465-470.
A 20-year review of central nervous system decompression sickness. "Inappropriate practices such as ….Non-treatment … resulted in a high incidence of deterioration or relapse".
Rivera JC: Decompression sickness among divers: an analysis of 935 cases. Military Medicine 1964:314-334.
The U. S. Navy’s experience, involving almost 1,000 cases. It, again, demonstrates the efficacy of immediate hyperbaric treatment.
Moon RE: Treatment of gas bubble disease. Problems in Respiratory Care 1991;4(2):232-252.
Comprehensive review article.
Moon RE, Sheffield PJ: Guidelines for treatment of decompression illness. Aviation, Space, and Environmental Medicine 1997;68(3):234-243.
Consensus statement/guidelines for the treatment of decompression sickness, based upon a scientific workshop involving an internationally-respected faculty. "Definitive treatment … incorporates compression and administration of breathing gas with elevated partial pressures of oxygen". "Rapid administration of pressure and oxygen is paramount …"
3. GAS EMBOLISM
Anon: U.S. Navy Diving Manual, Volume 1 (Air Diving) 1993, Revision 3:8-18--8-20. Best Publishing Co., Flagstaff, Arizona.
The authoritative text of the United States military government. It notes, among other things, that "… unless treated promptly and properly by recompression (hyperbaric oxygen therapy), arterial gas embolism is likely to result in death or permanent brain damage".
Anon: NOAA Diving Manual, Diving for Science and Technology 1991, 20-9--20-13.
The authoritative text of the United States civilian government. It states, among other things, that "Prompt recompression (hyperbaric oxygen therapy) is the only treatment for gas embolism".
Waite CL, Mazzone WF, Greenwood, ME, et al: Cerebral air embolism, I. Basic studies. Submarine Medical Research Laboratory, U.S. Naval Submarine Medical Center Report No. 493:1-14.
Historically significant publication from the U.S. Navy Bureau of Medicine and Surgery. It compares hyperbaric treatment to no hyperbaric treatment in an open-brain model of gas embolism. Dogs not treated hyperbarically "all died or were left with severe residual neurological defects". All of the hyperbarically-treated animals made a complete recovery, with one exception. This research paved the way for the modern hyperbaric treatment protocols for gas embolism.
Moon RE: Gas embolism. Handbook on Hyperbaric Medicine, Eds. Oriani G, Marroni A, Wattel F. Springer, Italy 1966:229-248.
Comprehensive review article.
Helps SC, Gorman DF: Air embolism of the brain in rabbits pretreated with mechlorethamine. Stroke 1991;22:351-354.
The third in a series of articles published in STROKE by these authors. They have demonstrated a more complex pathophysiology than that previously appreciated. Cerebral arterial embolization results in flow deficit, ischemia, followed by a reperfusion-like injury component in many cases. Such ischemia-reperfusion complications require the presence of leukocytes. Hyperbaric oxygen is necessary to support areas of critical flow impairment. Hyperbaric oxygen will also serve to antagonize leukocyte-mediate ishemic-reperfusion injury (see #5, Acute Traumatic Peripheral Ischemia, Article #9, Zamboni, et al).
Reasoner DK, Dexter F, Hindman BJ, et al: Somastosensory evoked potentials correlate with neurological outcome in rabbits undergoing cerebral air embolism. Stroke 1996;27(10):1859-1864.
Validation of the Helps and Gorman’s (above) model of using evoked potentials to correlate neurological outcome in gas embolism.
Kol S, Ammar R, Weisz G, et al: Hyperbaric oxygenation for arterial air embolism during cardiopulmonary bypass. Ann Thorac Surg 1993;55:401-403.
Representative paper addressing one of the many iatrogenic etiologies of gas embolism. It reports the morbidity and mortality associated with this complication when HBO therapy is not utilized. It further described the importance of early hyperbaric referral and treatment.
Bitterman H, Melamed Y: Delayed hyperbaric treatment of cerebral air embolism. Isr J Med Sci 1993;29(1):22-26.
A report of the efficacy of HBO therapy in reversal of latent coma, hemiplegia, and hemiparesis.
Leitch DR, Greenbaum LJ, Hallenbeck: Cerebral arterial air embolism: II. Effect of pressure and time on cortical evoked potential recovery. Undersea Biomed Res 1984;11(3):237-248.
Compares treatment protocols in a "severe" model of gas embolism " … no treatment surpassed oxygen at 2.8 bar" (hyperbaric oxygen therapy).
Leitch DR, Greenbaum, LJ, Hallenbeck: Cerebral arterial air embolism: IV. Failure to recover with treatment, and secondary deterioration. Undersea Biomed Res 1984;11(3):265-274.
Comparison of treatment protocols in a "severe" model of gas embolism. Hyperbaric doses of air and oxygen were compared to normobaric (non-hyperbaric) air. In extrapolating this model to the clinical arena "…the majority of patients with severe arterial gas embolism will achieve maximum benefit from compression to 2.8 bar while breathing oxygen", i.e.,hyperbaric oxygen therapy.
McDermott JJ, Dutka AJ, Koller WA, et al: Effects of an increased P02 during recompression therapy for the treatment of experimental cerebral arterial gas embolism. Undersea Biomed Res 1992;19(6):403-413.
Highly significant outcome improvement when two standard hyperbaric treatment protocols were compared to non-hyperbaric air.
Kearns PJ, Haulk AA, McDonald TW: Homonymous hemianopia due to cerebral air embolism from central venous catheters. The Western Journal of Medicine Case Reports 1984;140(4):615-617.
Reports the sustained neurological compromise (infarcts via C.T. scan) in patients with gas embolism not treated hyperbarically.
4. GAS GANGRENE
Bakker DJ: Clostridial myonecrosis. In Problem Wounds, The Role of Oxygen, Eds. Davis JC and Hunt TK 1988:153-172, Elsevier Publishing Co., New York.
A comprehensive review article from the institution that has pioneered the medical and surgical management of gas gangrene over the past four decades. This reported case series involving bacterially-proven clostridium perfringens gas gangrene is the largest in the world,. The report demonstrates that early application of HBO therapy:
- is life-saving
- is limb- and tissue-saving
- clarifies the demarcation
Van Unnik AJM: Inhibition of toxin production in Clostridium perfringens in vitro by hyperbaric oxygen. Antonie Van Leeuwenhoek 1965;31:181-186.
An historically important in-vitro study that demonstrated the critical role that Alfa-toxin plays in the pathophysiology of Clostridium perfringens (gas gangrene) infections. Further, HBO therapy inhibited production of this toxin.
Kaye D: Effect of hyperbaric oxygen on Clostridia in vitro and in vivo. Proc Soc Exp Biol Med 1967;124:360-366.
A second early study that confirmed the bactericidal properties of HBO therapy in gas gangrene. HBO was protective, resulting in decreased mortality.
Hart GB, Lamb RC, Strauss MB: Gas gangrene: I. A collective review. The Journal of Trauma 1983;23(11):991-1000.
This two-part report initially provides a 20-year literature review of gas gangrene, indicating that "a combined therapy approach with early recognition, surgical intervention, appropriate antibiotics, and hyperbaric oxygen (HBO) provides optimal care". The second part summarizes the outcomes of a large clinical series, supporting the earlier contention that the addition of HBO therapy to standard surgical and antibiotic regimes optimizes survival.
Demello FJ, Haglin JJ, Hitchcock CR: Comparative study of experimental Clostridium perfringens infection in dogs treated with antibiotics, surgery, and hyperbaric oxygen. Surgery 1973;73(6):936-941.
A comparative study of gas gangrene treated with various combinations of surgery, antibiotics and hyperbaric oxygen. Maximum effectiveness (95% survival) was achieved when all three modalities were combined.
Hirn M: Hyperbaric oxygen in the treatment of gas gangrene and perineal necrotizing fasciitis. Eur J Surg 1993;(570):1-36.
A monograph; it describes both an experimental model and a clinical series. The animal model resulted in statistically significant improvement in survival (13% vs. 38%) when HBO therapy was combined with surgical debridement. Clinically, HBO reduced mortality through multifactional mechanisms, which the author describes in detail.
Hirn M, Niinikoski J, Lehtonen OP: Effect of hyperbaric oxygen and surgery on experimental gas gangrene. Eur Surg Res 1992;24:356-362.
An experimental model of Clostridial gas gangrene that reflects modern day medical and surgical management practices. The findings are entirely consistent with historic data, in that the addition of HBO therapy reduced both morbidity and mortality.
5. ACUTE TRAUMATIC PERIPHERAL ISCHEMIA
Note: Within the Medicare 35-10 "Covered Conditions" listing are three conditions for which the rationale for HBO therapy is essentially identical. These conditions involve different etiologies but the net insult will frequently follow the common pathway of :acute ischemia; tissue hypoxia; threatened tissue viability; necrosis; reperfusion injury, and threatened limb loss.
These conditions are:
#5 Acute Traumatic Peripheral Ischemia
#6 Crush Injuries, and Suturing of Severed Limbs.
#8 Acute Peripheral Arterial Insufficiency
As a consequence of this common disease pathway, the supportive literature provided below can serve as representative of all three conditions.
Bouachour MD, Cronier P, Gouello JP, ET AL.: Hyperbaric oxygen therapy in the management of crush injuries: A randomized double-blind placebo-controlled clinical trial. The Journal of Trauma: Injury, Infection, and Critical Care 1996; 41(2): 333-339
A placebo-controlled randomized and blinded clinical trial in acute limb-threatening trauma to the extremities. Statistically significant improvement in outcome occurred in the HBO group. HBO therapy improved wound healing, reduced the number of surgical procedures, and likewise reduced the number of amputations that became necessary.
Strauss MB, Hart GB.: Crush injury and the role of hyperbaric oxygen. Topics in Emergency Medicine 1984; 6: 9-24
An early review article of HBO’s therapeutic impact in crush injury. It predated our knowledge of HBO’s effect on ischemia-reperfusion injury. Consequently, HBO’s role is even more comprehensivet than described herein.
Lemperle B: Hyperbaric oxygen therapy for treatment of crush injury and acute traumatic peripheral ischemia. Health Technology Assessment Report 1983, DHHS Publ. No. 84-3372:171-18
A United States Department Health and Human Services, "Health Technology Assessment Report." It concludes that "There appears to be a rational theoretical basis for using HBO as an adjunctive treatment for crush injury and acute traumatic ischemia…". Again, this report predates our understanding of the important role that HBO plays in ischemia-reperfusion injury. A more recent edition of this report would likely conclude that HBO therapy is tissue sparing/limb salvaging.
Nylander G, Otamiri T, Lewis DH, ET AL.: Lipid peroxidation products in postischemic skeletal muscle and after treatment with hyperbaric oxygen. Scandinavian Journal of Plastic Reconstructive Surgery 1989; 23: 97-103
Early basic science evidence of a therapeutic effect of HBO therapy in post-ischemia muscle tissue.
Skyhar MJ, Hargens AR, Strauss MB, ET AL.: Hyperbaric oxygen reduces edema and necrosis of skeletal muscle in compartment syndromes associated with hemorrhagic hypotension. Journal of Bone and Joint Surgery 1986; 68A: 1218-1224
Further laboratory evidence of the multi factorial benefits that HBO therapy imparts in acute ischemia/compartment syndrome.
Nylander G. Lewis D. Nordstrom H, ET AL.: Reduction of postischemic edema with hyperbaric oxygen. Plastic and reconstructive surgery 1985; 76(4): 596-601
The consistent laboratory finding of improved outcomes following acute peripheral ischemia and treatment with HBO.
Thom SR, Mendiguren I, Hardy K, ET AL.: Inhibition of human neutrophil B2-integrin-dependent adherence by hyperbaric o2. AM J Physiol 1997; 272 (Cell Physiol. 41): C 770-C777
This paper is included here to demonstrate the depth at which researchers have investigated in order to elucidate HBO’s therapeutic effects in ischemia-reperfusion injury.
Strauss MB, Hargens AR, Gershuni DH, ET AL.: Reduction of skeletal muscle necrosis using intermittent hyperbaric oxygen in a model compartment syndrome. The Journal of Bone and Joint Surgery 1983; 65-A: 656-662
Further basic science to support the clinical application of HBO therapy in acute peripheral ischemias: compelling histological evidence of benefit.
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; 91(6): 1110-1123
Using modern-day laboratory techniques, this work provides firm morphologic evidence of the beneficial effect of HBO therapy on microcirculatory perfusion in ischemia-reperfusion injury. HBO therapy is observed to protect the microcirculation from an otherwise post ischemia reperfusion injury.
Nylander G, Nordstrom H, Lewis D, ET AL. Metabolic effects of hyperbaric oxygen in postischemic muscle. Plastic and Reconstructive Surgery 1987; 79(1): 91-97
Sub-cellular evidence of therapeutic effects associated with the application of hyperbaric hyperoxia in post-ischemic muscle tissue. The authors conclude that "Hyperbraic oxygen treatments in the post-ischemic phase stimulate aerobic metabolism."
Radonic V, Baric D, Giunio L, ET AL.: War injuries of the femoral artery and vein: A report on 67 cases. Cardiovascular Surgery 1998; 5 (6): 641-647
A clinical series of war wounded patients. "Hyperbaric oxygen therapy should be used in selected cases in order to improve tissue oxygenation, wound healing, host defense mechanisms, and therapy."
Shupak A, Gozal D, Melaned AY, ET AL. Hyperbaric oxygenation in acute peripheral posttraumatic ischemia. Journal of Hyperbaric Medicine 1987; 2 (1): 7-14
A second clinical series of patients suffering acute post-traumatic limb ischemia. The authors stress the important adjunctive role of HBO therapy.
6. PROGRESSIVE NECROTIZING INFECTION
Green RJ, Dafoe DC, Raffin TA: Necrotizing fasciitis. Chest 1996;110(1)219-229.
A recent review of necrotizing fasciitis, published in CHEST. With regard to hyperbaric oxygen, the authors conclude that where available, "it should be considered as a treatment adjunct in patients with necrotizing fasciitis".
Knighton DR, Halliday B, Hunt TK: Oxygen as an antibiotic: the effect of inspired oxygen on infection. Arch Surg 1984;119:199-204.
This reference is included to emphasize an important feature of HBO therapy in infectious diseases. Hyperbaric doses of oxygen take on antibiotic-like properties. The paper stresses the importance of sufficient local oxygen tension in order that bacterial killing by leukocytes can be accomplished.
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.
The same authors cited in the previous paper demonstrate an additive effect when elevated oxygen tensions are combined with antibiotics.
Mader JT, Guckian JC, Glass DL, et al: Therapy with hyperbaric oxygen for experimental osteomyelitis due to staphylococcus aureus in rabbits. The Journal of Infectious Diseases 1978;138(3):312-318.
The third of three papers that provide important mechanistic support for HBO therapy in infected tissue. In this case, HBO improves leukocyte antimicrobial function.
Bakker DJ: Pure and mixed aerobic and anaerobic soft tissue infections. Hyperbaric Oxygen Review 1985;6(2):65-96.
A review article, with emphasis on the role of hyperbaric oxygen therapy. The author further presents 50 cases from his institution.
Hirn M: Hyperbaric oxygen in the treatment of gas gangrene and perineal necrotizing fasciitis. Eur J Surg 1993;(570):1-36.
A monograph; it describes an experimental model of both necrotizing fasciitis and gas gangrene, a clinical series, and a literature review. HBO therapy decreases mortality, clarifies the demarcation of necrotic vs. potentially viable tissue (improved limb salvage), and enhances wound healing.
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.
A clinical study of 29 patients, in which outcome was compared between a surgery and antibiotics group and a surgery, antibiotics, and HBO therapy group. The addition of HBO "… significantly reduced mortality and wound morbidity/number of treatments".
Gozal D, Ziser A, Shupak A, et al: Necrotizing fasciitis. Arch Surg 1986;121:233-235.
A small clinical series in which the combined approach of surgery, antibiotics and HBO therapy resulted in a mortality of 12.5%. This compared with mortality rates as high as 72.7% noted in the paper’s review of the disease treated without HBO.
Pizzorno R, Bonini F, Donelli A, et al: Hyperbaric oxygen therapy in the treatment of Fournier’s disease in 11 male patients. The Journal of Urology 1997;158:837-840.
A clinical series of the "Fournier’s Disease" aspect of necrotizing soft tissue infections. The authors, while recognizing their small number of patients, felt that their results "underline the importance of hyperbaric oxygen therapy …"
Hollabaugh RS, Dmochowski RR, Hickerson EL, et al: Fournier’s gangrene: therapeutic impact of hyperbaric oxygen. Plast. Reconstr. Surg. 1998;101(1):94-100.
A very recent clinical series involving two largely equal groups, with HBO therapy as the variable. Mortality was 7% in the HBO group compared to 42% in those not receiving HBO (statistical significance at the 0.05 level).
McHenry CR, Piotrowski JJ, Petrinic D, et al: Determinants of mortality for necrotizing soft-tissue infections. Ann. Surg. 1995;221(5):558-565.
Contrast the previous papers with that presented in this oft-quoted paper that reported improved mortality (29%!) vs. previous literature. The authors discounted HBO therapy’s efficacy and suggested that its use will delay debridement. Typically, HBO therapy does not precede surgery, therefore, such delays do not occur.
7. PREPARATION AND PRESERVATION OF COMPROMISED SKIN GRAFT
Note
Problem wound healing frequently occurs in patients who are systemically or locally host compromised. Regardless of underlying etiology, tissue hypoxia is the most common denominator. When operative repair is necessary, surgeons turn to the Reconstructive Ladder, a series of graft and flap options of increasing complexity.
For skin grafts to be considered, the recipient bed must be of the health and quality to accept and nourish a graft. This is critical, as such grafts are immediately rendered ischemic/hypoxic upon harvest.
Availability of oxygen is critical to the success of any skin grafting procedure, and subsequent graft durability. The following papers chronicle the role of oxygen in the healing process, and conclude with the application of HBO therapy in wound healing and limb salvage. Such application is designed to either:
- prepare the recipient bed for definitive coverage (grafts or flaps)
- it is recognized that, in some cases, the therapeutic effect of HBO will be such that skin grafting may be unnecessary.
- support skin graft or skin flap procedures, in the immediate post-operative setting.
Sheffield PJ: Tissue oxygen measurements with respect to soft-tissue wound healing with normobaric and hyperbaric oxygen. HBO Review 1985;6(1):18-43.
Evidence that hyperbaric doses of oxygen increase tissue oxygen levels in otherwise hypoxic and ischemic wounds. This work represents a fundamental rationale for the application of HBO therapy in the setting of non-healing lesions, where an underlying hypoxia is demonstrated.
Padberg FT, Back TL, Thompson PN, et al: Transcutaneous oxygen (TcP02) estimates probability of healing in the ischemic extremity. J Surg Res 1996;60(2):365-369.
A more recent evaluation of the relationship between availability of oxygen and probability of healing in the ischemic extremity. Transcutaneous oximetry "alone" is sufficient for objective risk stratification of arterial ischemia in the lower extremity.
Bunt TJ, Holloway GA: TcP02 as an accurate predictor of therapy in limb salvage. Ann Vasc Surg 1996;10(3):224-227.
Further evidence of both the role of oxygen in limb salvage, and the ability of transcutaneous oximetry to identify tissue beds at risk.
LaVan FB, Hunt TK: Oxygen and wound healing. Clinics in Plast Surg 1990;17(3):463-472.
This paper summarizes the extensive amount of basic research (much of which came from these authors’ laboratory at the University of California, San Francisco). The authors emphasize the role of HBO therapy as a "strong stimulus" for angiogenesis. They further note that HBO is not effective "if blood supply is insufficient". Hence, the important role of transcutaneous oxygen in the case management of hyperbarically-referred patients under the Preparation or Preservation of Compromised Graft protocol.
Clarke D: An evidence-based approach to hyperbaric wound healing. Blood Gas News 1998;7(2):14-20.
One example of an algorithmic approach to hyperbaric wound healing. The goal is to identify those who possess the physiologic capability to respond locally (the wound) to centrally-delivered (HBO) hyperoxia. In those patients, determination of therapeutic endpoint (when a critical mass of angiogenesis is presumed to be present) ensures a cost-effective application of this therapeutic resource.
Tompach PC, Lew D, Stoll JL: Cell response to hyperbaric oxygen treatment. Int J Oral Maxillofac Surg 1997;26:82-86
More advanced thinking, and confirmatory study, regarding the effect of HBO on wound healing. Here, in an in-vitro cell model, HBO positively influences healing responses at the cellular level.
Hehenberger K, Brismar K, Lind F, et al: Dose-dependent hyperbaric oxygen stimulation of human fibroblast proliferation. Wound Rep Reg 1997;5(2):147-150.
Further cellular research that demonstrates the dose dependent nature of oxygen on an important component of the wound healing module.
Siddiqui A, Davidson JD, Mustoe TA: Ischemic tissue oxygen capacitance after hyperbaric oxygen therapy: A new physiologic concept. Plast Reconstr Surg 1997;99(1):148-155.
A new concept is proposed, one that incorporates previous evidence of HBO’s benefit in ischemic wound healing, and is supported by the research presented herein. This work further demonstrates the superiority of hyperbaric vs. normobaric oxygen.
Gibson JJ, Hunt TK: Hyperbaric oxygen potentiates wound healing. Diving and Hyperbaric Medicine Proc. 23rd EUBS Congress, Bled. Slovenia 1997:153-160.
This paper demonstrates a beneficial effect of HBO therapy, in a dose-dependent manner, on angiogenesis. This effect is highly significant when compared to "controls"; air breathing at sea level pressure.
Boykin JV: Hyperbaric oxygen therapy: A physiological approach to selected problem wound healing. Wounds 1996;8(6):183-198.
A recent summary article of the role of HBO therapy in problem wound healing. This paper captures much of the historic and recent science, and molds it into a clinical algorithm in order to maximize medical and surgical management.
Hammarlund C, Sundberg T: Hyperbaric oxygen reduced size of chronic leg ulcers: A randomized double-blind study. Pjlast Reconstr Surg 1994;93(4):829-833.
An exacting clinical study. The wounds in question had failed to heal over more than one year. The healing effect of HBO on these ulcers was highly significant (p<0.001).
Baroni G, Porro T, Faglia E, et al: Hyperbaric oxygen in diabetic gangrene treatment. Diabetes Care 1987;10(1):81-86.
One of the "early" case controlled studies, in which HBO was evaluated in diabetic foot gangrene. It was not uncommon for these patients to undergo subsequent grafts or flap repair, in one form or another, when major limb salvage is averted. HBO therapy markedly reduced the rate of such amputations.
Oriani G, Michael M. Meazza D, et al: Diabetic foot and hyperbaric oxygen therapy: A ten-year experience. J Hyperbaric Med 1992;7(4):213-221.
A similar study, and findings, to the previous paper. Diabetic foot ulcers benefited from HBO pre-operatively.
Faglia E, Favales F, Aldeghi A, et al: Adjunctive systemic hyperbaric oxygen therapy in treatment of severe prevalently ischemic diabetic foot ulcer. Diabetes Care 1996;19(12):1338-1343.
A randomized controlled clinical trial; the findings of which mirror those of the two previous, and less well controlled, reports. Note that transcutaneous oxygen data was able to discriminate between the healed and non-healed groups.
Wheen L: The effectiveness and cost of oxygen therapy for diabetic foot wounds. SPUMS Journal 1994;24(4):182-190.
A paper that evaluates the clinical and cost-effectiveness of HBO therapy in diabetic foot wounds. "…the financial costs are lessened when hyperbaric oxygen therapy is used in combination with conventional management of the problem diabetic foot".
Bowersox JC, Strauss MB, Hart GB: Hyperbaric oxygen treatment in the management of threatened skin flaps and grafts. Handout: VIII International Congress on HBO, Long Beach, California 1984:149-152.
A report of the application of HBO therapy in threatened skin flaps/skin grafts. "…90% of the patients with grafts had risk factors that were considered poor prognostic signs". Almost all of these risks involved resulted in an underlying hypoxic component (PVD, radiation therapy to the recipient bed, diabetes mellitus). Presumably, if transcutaneous oximetry had been afforded these patients, many graft or flap procedures would have been deferred pending a pre-operative course of HBO therapy! Here is evidence of the high failure rate of graft/flap procedures in tissue beds previously rendered hypoxic.
Perrins, DJF: Influence of hyperbaric oxygen on the survival of split skin grafts. The Lancet 1967:868-871.
The first controlled study of HBO therapy in skin graft support. HBO therapy resulted in twice as many graft "takes" than the control group.
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. J Reconst Microsurg 1989;5(4):343-347.
HBO therapy is observed to increase axial pattern skin flap survival when administered during or immediately after total flap ischemia. The administration of HBO during ischemia with resulting improved outcome was surprising at the time of this publication. These authors have since demonstrated a "constitutional" effect of HBO, influencing the ischemia-reperfusion syndrome in a way that minimizes/negates I-R injury.
Kaelin CM, Im MJ, Myers RA, et al: The effects of hyperbaric oxygen on free flaps in rats. Arch Surg 1990;125:607-609.
The "pre-operative" benefits of HBO therapy in flap reconstruction.
Stevens DM, Weiss DD, Koller WA, et al: Survival of normothermic microvascular flaps after prolonged secondary ischemia: Effects of hyperbaric oxygen. Otolaryngol Head Neck Surg 1996;115(4):360-364.
A study that closely equates to the clinical setting; i.e., flap repair (including a "primary" ischemic period), flap ischemic compromise with resulting secondary ischemia, then correction of secondary ischemia with resulting reperfusion. HBO, but not normobaric oxygen, therapy enhanced flap tolerance, and survival. "… the additional expense and technology of a hyperbaric chamber system is necessary to achieve this effect.
Note
This final paper is included to show the consequences of a failure to incorporate exacting patient selection, and an algorithmic approach to hyperbaric wound healing. The reviewer must, however, also read the rebuttal "Letter-to-the-Editor" that immediately follows this paper, to appreciate the distinction in the way that this center operated, and the way it should have operated.
Ciaravino ME, Friedell ML, Kammerlocher TC: Is hyperbaric oxygen a useful adjunct in the management of problem lower extremity wounds? Ann Vasc Surg 1996;10(6):558-562.
8. MANDIBULAR OSTEORADIONECROSIS
Myers RAM, Marx RE: Use of hyperbaric oxygen in postradiation head and neck surgery. NCI Monogr 1990; 9: 151-157
One paper from the proceedings of the National Cancer Institute Consensus Development Conference on Oral Complications of Cancer Therapies: Diagnosis, Prevention, and Treatment. This paper clarified the pathophysiology of radiation-induced tissue injury, and the evidence supporting a peri-operative role for hyperbaric oxygen therapy. One significant consequence of this paper was that the resulting National Cancer Institute Consensus Statement included the following statements:
" Early stages of ORN (osteoradionecrosis) without fractures or fistulae may be cured by HBO (hyperbaric oxygen therapy) alone. More advanced cases require, in addition to HBO, sequestrectomy or partial mandibulectom,y with eventual bare grafting."
" For patients who are thought to be particularly high risk of developing ORN, prextraction HBO should be considered."
The consensus statement ended with a series of ‘Conclusions and Recommendations’. A particular reference to HBO was the following:
ORN can be prevented. When present, it is best managed with HBO alone or with surgery".
National Institutes of Health Consensus Development Panel. Consensus statement: Oral complications of cancer therapies. NCI Monographs 1990; 9: 3-9 Consensus Development Conference.
The entire NCI consensus statement is included.
Marx RE: Osteoradionecrosis: A new concept of its pathophysiology. J Oral Maxillofac Surg 1983; 41: 283-288
A landmark publication, in that it clarified the underlying pathophysiological process of late radiation tissue injury. This data paved the way for studies, many conducted by the same author(s), to determine the therapeutic mechanism of HBO (see next paper)
Marx RE: A new concept in treatment of osteoradionecrosis. J Oral Maxillofac Surg 1983; 41:351-357
ORN was long considered an osteomyelitis process (infection of compromised bone by invading organisms). This research, based on the above pathophysiology, produced a peri-operative algorithmically based HBO protocol. This "Marx Protocol" drives the modern application of HBO Therapy in ORN.
Marx RE, Johnson RP, Kline SN: Prevention of osteoradionecrosis: A randomized prospective clinical trial of hyperbaric oxygen versus penicillin. JADA 1985; 111: 49-54.
Following the above referenced research, it was further demonstrated that ORN could be prevented by the prophylactic use of HBO therapy, but not by penicillin (previously thought to be beneficial). Further support of the enlighten appreciation of the underlying pathophysiology of the disease, and the therapeutic benefit of HBO.
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
This study compared hyperbaric oxygen to normobaric oxygen (100% oxygen breathing in a non-hyperbaric setting. i.e. one that could be achieved in the normal clinical setting) to normobaric air (what the reader is presumably breathing). It was the hyperbaric environment, with oxygen breathing, that resulted in angiogenesis within previously irradiated tissue. The evidence was statistically significant when compared to oxygen and air breathing at normal atmospheric pressure.
Marx RE, Kindwall EP: Radiation injury to tissue. Hyperbaric Medicine Practice 1995; 23: 447-503
Detailed overview of ORN. This paper further reports the results of a randomized prospective study (pages 464-468. Of equal importance, perhaps, will be the impressive cost savings associated with the Marx protocol (the peri-operative staging of HBO based upon extent of ORN - and consistent with the National Cancer Institute Consensus Statement, pages 486-498).
Granstrom G, Devge C, Tjellstrom: Laser doppler flowmetry for the intraosseous blood flow measurement after irradiation, bone grafting and hyperbaric oxygen treatment. Proceedings of the XIXth annual meeting of EUBS 1993, Trondheim Norway.
The reviewers attention is directed to this publication as it is the first reported evidence that HBO induces angiogenesis in bone, as well as soft tissue. These authors are internationally respected basic and applied researchers and clinicians. It is typical for their data to be first published as Proceedings, as is the case here. They subsequently move on to indexed and peer review publications, as will be apparent in several of the following citations.
Granstrom G, Bergstrom K, Tjellstrom A, et al: A detailed analysis of titanium implants lost in irradiated tissues. The International Journal of Oral and Maxillofacial Implants 1994; 9: 653-662
A case controlled study of the effect of HBO on titanium implant loss in radiation-injured facial bones (ORN). Preoperative HBO improved the osseointegration of implants. Statistical significance is evident when implant loss is compared with and without HBO.
Granstrom G: Osseointegration in the irradiated patient. Osseointegration in Craniofacial Reconstruction; Eds. P-I Branemark & D. Tolman, Quintessence Publ. 1998:95-108
A very recent publication which serves to comprehensively review the role of HBO in radiation-damaged facial bones. Several hundred patients are involved in this group’s experience. Clinical and economic outcomes are presented.
Mealey BL, Semba SE, Hallmon WW: The head and neck radiotherapy patient: part 2- management of oral complications. Compend. Contin. Educ. Dent. 1994; 15 (4): 442-485
A "Dental Continuing Education" series. This represents an important teaching/ continuing education vehicle for practicing dentists. As noted, a key learning objective is to explain the role of hyperbaric oxygen therapy in prevention and treatment of osteoradionecrosis. Examples, from the text, include:
"Hyperbaric oxygen therapy has been found particularly helpful in the treatment of large areas of necrosis…"
"…HBO therapy improved the healing capacity of the remaining tissues."
Mckenzie MR, Wong FLW, Epstein JB, et al: Hyperbaric oxygen and postradiation osteonecrosis of the mandible. Oral Oncology, European Journal of Cancer. 1993; 29B(3): 201-207
A representative paper reporting a clinical series of 26 cases diagnosed with ORN and treated hyperbarically; complete resolution occurred in 23 of 26 patients.
Epstein H, Van Der Meij E, Mckensie M, et al: Hyperbaric oxygen therapy: Letter to the editor. Oral Surgery Oral Medicine Oral Pathology 1996;81(3):265-266.
A clinical and economic summary involving 12 episodes of ORN that had failed to heal. Prior treatments involved antibiotics, oral rinses, debridement, and sequestrectomy. All healed following the employment of HBO alone or in conjunction with repeat surgeries. This paper, which involves the British National Health System, concluded that HBO was "cost-effective" when used within a hospital setting. Interestingly, this cost-effective determination did not take into account the costs associated with all previously failed medical and surgical interventions.
Dempsey J, Haynes N, Smith T, et al. Cost effectiveness analysis of hyper-baric therapy in osteoradionecrosis. Can. J. Plast. Surg. 1997; 5(4): 221-229
An economic evaluation of the use of HBO in osteoradionecrosis. The detail of this study is such that even the daily parking expenses of the hyperbaric group were taken into consideration. The final analysis was that it is six times more expensive not to use HBO.
9. SOFT TISSUE RADIONECROSIS
Note
The following papers represent a broad range of anatomic sites that commonly suffer tissue breakdown and loss as a consequence of radiation tissue injury. The pathophysiology associated with such injury is found to be largely identical to that which complicates bony tissue (osteoradionecrosis).
Kindwall EP: Hyperbaric oxygen’s effect on radiation necrosis. Clinics in Plastic Surgery 1993;20(3):473-483.
A comprehensive review, directed at the Plastic Surgery specialty.
Anon.: Hyperbaric oxygen therapy for treatment of soft tissue radionecrosis and osteoradionecrosis. Health Technology Assessment Reports 1982; DHHS Publication No. (PHS) 84.3371.
A United States Department of Health and Human Services Public Health Service "Health Technology Assessment Report" on the Treatment of Soft Tissue Radionecrosis …" Even as early as 1982 this report concluded that "there is little controversy in the medical community regarding the safety and effectiveness of HBO as an adjunctive therapy in the treatment of soft tissue radionecrosis…" Of course, in 1999 we have a greater appreciation of the precise pathophysiology of this disorder. So, too, the therapeutic effects of HBO therapy. Equally important is the evolution to a protocol-driven approach, in common practice today.
Neovius EB, Lind MG, Lind FG: Hyperbaric oxygen therapy for wound complications after surgery in the irradiated head and neck: a review of the literature and a report of 15 consecutive patients. Head & Neck 1997;19:315-322.
A literature review, from a hyperbaric perspective, involving head and neck radionecrosis. The authors then report their own clinical experiences, and conclude that HBO therapy has "a clinically significant effect on initiation and acceleration of healing processes …"
"Feldmeier JJ, Heimbach RD, Davolt DA, et al.: Hyperbaric oxygen as an adjunctive treatment for severe laryngeal necrosis: a report of nine consecutive cases. Undersea & Hyperbaric Med 1993;20(4):329-335.
The authors summarize their experience with laryngeal radionecrosis in nine patients. Notably, none of the nine patients required laryngectomy.
Samuels L, Granick MS, Ramasastry S, et al: Reconstruction of radiation-induced chest wall lesions. Ann Plast Surg 1993;31(5):399-405.
This paper is included in order to sensitize the reviewer to the enormous complications associated with repair of soft tissue radionecrosis without the benefit of perioperative HBO therapy. Modern reconstructive techniques were employed, and had to be repeated in several cases. The underlying problem of radiation-induced endarteritis dogged these procedures. Repeat and costly surgeries were necessary, essentially debriding the entire "radiation portal" of soft tissue in some instances. Two patients were left with non-healing wounds, another six (29%) suffered flap compromise (expensive failures!).
Feldmeier JJ, Heimbach RD, Davolt DA, et al: Hyperbaric oxygen as an adjunctive treatment for delayed radiation injury of the chest wall: a retrospective review of twenty-three cases. Undersea & Hyper Med 1995;22(4):383-393.
In contrast to the above article, improved outcomes resulting from the repair of chest wall defects are reported, when HBO therapy is incorporated into the treatment plan.
Bevers RFM, Bakker DJ, Kurth KH: Hyperbaric oxygen treatment for haemorrhagic radiation cystitis. The Lancet 1995;346:803-805.
A relatively large series of patients suffering radiation-induced cystitis, and treated hyperbarically. The paper notes the ineffectiveness of non-hyperbaric medical and surgical strategies. The impressive outcomes (37 of 40 patients healed) contrast sharply with previously reported case series, when patients were not afforded HBO therapy.
Rijkmans, BG, Bakker DJ, Dabhoiwala NF, et al: Successful treatment of radiation cystitis with hyperbaric oxygen. Eur Urol 1989;16:354-356.
Another clinical series in which HBO therapy was found effective. Interestingly, and as an aside, the use of HBO hastened the diagnosis of recurrent bladder tumor. Biopsy of radionecrotic bladder is largely hit or miss. Following a course of HBO therapy, the bladder wall normalizes in all areas except those involving tumor, making subsequent biopsies of suspected lesions more precise. This has critically important implications, of course. Those so identified will stand to benefit from earlier anti-cancer care.
Lee HC, Liu CS, Chiao C, et al: Hyperbaric oxygen therapy in hemorrhagic radiation cystitis: a report of 20 cases. Undersea Hyperbaric Med 1994;21(3):321-327.
Excellent to good (halted to markedly decreased hemorrhagic cystitis) outcomes in 90% of patients whose previous medical and surgical care had failed to resolve this radiation-induced complication.
Williams JA, Clarke D, Dennis WA, et al: The treatment of pelvic soft tissue radiation necrosis with hyperbaric oxygen. Am J Obstet Gynecol 1992; 167(2): 412-416.
Gynecologic soft tissue radionecrosis successfully treated with HBO therapy. All patients had failed three months of other medical and surgical therapies.
Feldmeier JJ, Heimbach RD, Davolt DA, et al: Hyperbaric oxygen an adjunctive treatment for delayed radiation injuries of the abdomen and pelvis. Undersea Hyperbaric Med 1996;23(4):205-213.
A more recent publication again addressing pelvic and abdominal soft tissue radionecrosis. Providing that an "appropriate" course of HBO therapy was employed, healing of these complex complications of therapeutic radiotherapy occurred in 81% of 41 patients.
Fine BA, Hempling RE, Piver MS, et al: Severe radiation morbidity in carcinoma of the cervix: impact of pretherapy surgical staging and previous surgery. Int. J. Radiation Oncology Biol. Phys. 1995;31(4):717-723.
The reader is referred to this publication for the express purpose of appreciating the "severe radiation morbidity …" associated with carcinoma of the cervix. This involved 66 of 189 patients (34.9%). As with the two previous papers this work identifies the failure of medical and surgical plans that do not involve peri-operative HBO therapy.
Reedy MB, Capen CV, Baker DP, et al: Hyperbaric oxygen therapy following radical vulvectomy: an adjunctive therapy to improve wound healing. Gynecologic Oncology 1994;53:13-16.
HBO therapy, employed in a prospective observational manner, resulted in a reduction in wound breakdown and a shorter hospital stay.
10. CYANIDE POISONING
Hall AH, Rumack BH: Clinical toxicology of cyanide. Ann Emerg Med 1986;15:1067-1074.
A comprehensive review of the subject, written by Rocky Mountain Poison and Drug Center physicians (highly respected national experts on poisoning and overdoses). With regard to its treatment the authors advocate HBO therapy, particularly when supportive measures, and other cyanide antidotes fail.
Gonzales J, Sabatini S: Cyanide poisoning: pathophysiology and current approaches to therapy. The Internat J Artificial Organs 1989;12(6):347-355.
A second review, in which the authors again recommend the use of HBO therapy in selected cases. Given the date of this paper (1969) the authors rule out its use in infants and children due to potential risk factors, (risks not borne out in modern hyperbaric practice).
Cope C: The importance of oxygen in the treatment of cyanide poisoning. JAMA 1961;175(12):109-112.
In a cyanide poisoned animal model, the protective effect of oxygen on cardiac tissue is demonstrated. The author emphasizes the "paramount importance of including oxygen in the immediate treatment. It is noteworthy that oxygen administration is advocated even though hypoxia/anoxia is histotoxic. It is further reported that "oxygen is not only important, but indeed a specific antidote in cyanide poisoning".
Way JL, Gibbon SL, Sheehy M: Effect of oxygen on cyanide intoxication. I. Prophylactic protection. The J Pharm and Experimental Therapeutics 1966;153(2):381-385.
Another animal model of cyanide poisoning, in which the authors conclude "when it is employed in combination with other cyanide antagonist(s), oxygen potentiates the effectiveness of sodium nitrite and sodium thiosulfate".
Takano T, Miyazaki Y, Nashimoto I, et al: Effect of hyperbaric oxygen on cyanide intoxication: in situ changes in intracellular oxidation reduction. Undersea Biomed Res 1980;7(3):191-197.
This study was specifically designed to study the effect of HBO therapy in a model of cyanide poisoning. "It appears that oxygen has an antidotal potency when the dose of cyanide is at the critical, or just over the critical, level for mitochondrial respiratory function". "We consider that clinical administration of hyperbaric oxygen at a mild pressure represents a significant treatment if proper chemical treatment is carried out concomitantly".
Davis FM, Ewer T: Acute cyanide poisoning: case report of the use of hyperbaric oxygen. J Hyper Med 1988;3(2):103-106.
A case report, in which initial measures appeared to fail, but that "full consciousness was regained rapidly during the first 20 minutes (of) HBO". The patient made an uneventful recovery.
Sheehy M, Way JL: Effect of oxygen on cyanide intoxication. III. Mithridate. J Pharmacol Exp Therap 1968;161(1):163-168
An in-vivo study, evaluating the effects of oxygen on cyanide intoxication. The authors note that oxygen "strikingly potentiates the antidotal effect of sodium thiosulfate …"
11. ACTINOMYCOSIS
Mader JT, Wilson KJ: Actinomycosis: a review and the utilization of hyperbaric oxygen. HBO Review 1981;2(3):177-188.
A comprehensive review of this condition. The rationale for the adjunctive use of HBO therapy is described. High doses of oxygen impart a direct, as well as indirect, therapeutic effects. Production of oxygen-free radicals associated with hyperbaric-hyperoxia will overwhelm this anaerobes defenses, anaerobes which lack superoxide dismutase and catalse. High dose oxygen will also correct tissue hypoxia, the medium for growth of these infective organisms.
Manheim SD, Voleti C, Ludwig A, et al: Hyperbaric oxygen in the treatment of actinomycosis. JAMA 1969;210(3):552-553.
The first such case report in the English literature. HBO therapy was incorporated into the treatment plan following a several-month period of non-response to surgical excision, debridement, and antibiotic therapy, "the patient showed dramatic improvement", upon starting HBO.
Shauly Y, Nachum Z,Gdal-On M, et al: Adjunctive hyperbaric oxygen therapy for actinomycotic lacrimal canaliculitis. Graefe’s Arch Clin Exp Ophthalmol 1993;231:429-431.
A most recent case review, again involving a patient who was refractory to surgical excision and antibiotic therapy over a three-year period. "Complete cure was achieved only after hyperbaric oxygen therapy was added".
Anon.: Assessment of hyperbaric oxygen for treatment of actinomycosis. Health Technology Assessment Reports 1983. DHHS Publication No. (PHS) 84-3372:97-107.
This United States Department of Health and Human Services "Health Technology Assessment Report" summarizes the role of HBO therapy in the treatment of actinomycosis. The report is dated (1983), hence the apparent undue concern for safety of patients treated hyperbarically. An impressive safety record now characterizes the use of HBO therapy throughout North America. The report notes the infrequent occurrence of this disease, and recognizes that cases do occur that are refractory to both antibiotics and surgical management. Because of the lack of wide geographic availability of HBO therapy, few such refractory cases have been referred and treated. The hesitancy in fully endorsing HBO therapy in this report is based largely on the lack of extensive clinical experience/controlled trials. Given the infrequency of its occurrence, and greater infrequency of it becoming refractory, large case series are unlikely to be accumulated involving any therapy. When HBO has been incorporated it has been uniformly successful.