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The Center for Wound and Hyperbaric Medicine Idaho Elks Rehabilitation Hospital St. Luke's Health System
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Glossary of Terms

Acute Cyanide Poisoning
Acute cyanide poisoning as a pure toxicity is rare but has been reported to respond with benefit to hyperbaric oxygen in some cases. The primary, established therapy is chemical induction of 30 to 40 percent methemoglobinemia by administration of amyl nitrite and sodium nitrite with sodium thiosulfate. Nontoxic cyanomethemoglobin and thiocyanate are formed when methemoglobin and thiosulfate bind cyanide. Unfortunately, this treatment itself decreases the oxygen carrying capacity of the blood, and can cause tissue hypoxia which may require treatment. The serious nature of the condition warrants whatever other means may contribute to a more favorable prognosis (when conventional methods prove inadequate).

In combined carbon monoxide and cyanide smoke inhalation, oxygen diffusion may be impaired by pulmonary damage and caroboxyhemoglobinemia may compound the clinical crisis. In the presence of methemoglobinemia, inadequate tissue oxygenation is inevitable.

In combined carbon monoxide and cyanide poisoning which may accompany smoke inhalation, established treatment may have limited benefit. The physical and physiological rationale of mass action for hyperbaric oxygen in cyanide poisoning is very compelling. Results from the animal studies cited have shown distinct benefit from hyperbaric oxygen in this toxicity.

Cyanide is one of the most poisonous and rapidly acting substances known to man, with death occurring within seconds from a 100 mg inhaled dose and within a few hours from a 300 mg oral dose. Exposure generally occurs from smoke inhalation, because cyanide is a common product of combustion of many organic materials. Less commonly, cyanide poisoning can occur from occupational contact with the cyanide used in industrial processes such as electroplating; from iatrogenic exposure to sodium nitroprusside, a clinical hypotensive agent; and from suicide attempts. Smoke inhalation carries the additional co-morbidities of pulmonary injury, thermal burns, and carbon monoxide poisoning which has a synergistic toxic effect with cyanide. Cyanide (CN) produces a tissue hypoxia similar to the more common carbon monoxide (CO) poisoning, though without binding to hemoglobin. which are less toxic products.

HBOT provides an alternate pathway to the transport of oxygen to the tissues by increasing the serum dissolved oxygen to levels adequate for life, and thereby bypassing bound hemoglobin. HBOT is also the only treatment that directly reconstitutes the cytochrome A3 oxidase, and directly improves functioning of the electron transport system.

References

Birky MM, Clarke FB: Inhalation of toxic products from fires. Bull NY Acad Med 57:997-1013, 1981.

Burrows GE, Way JL: Cyanide intoxication in sheep: therapeutic value of oxygen or cobalt. Am J Vet Res 38:223-227, 1977.

\Clark CJ, Campbell D: Blood carboxyhemoglobin and cyanide levels in fire survivors. Lancet 1:1332-1335, 1981.

Cope C, Abramowitz S: Respiratory responses to intravenous sodium cyanide, a function of the oxygen-cyanide relationship. Am Rev Respir Dis 81:321-329, 1960.

Cope C: The importance of oxygen in the treatment of cyanide poisoning. JAMA 175:1061-1064.

Cottrell JE, Casthely J: Prevention of nitroprusside induced cyanide toxicity with hydroxocobalamin. N Engl J Med 298 (15):809-811, 1978.

Fassett DW: Cyanides and nitrites. In Patty FA (ed): Industrial Hygiene and Toxicology, Vol II. New York: Interscience Publishers, 1963, pp 2455-2456.

Hart GB, Strauss MB: Treatment of smoke inhalation by hyperbaric oxygen. J Emer Med 3(3):211-215, 1985.

Isom GE, Way JL: Effect of oxygen on cyanide intoxication. VI. Reactivation of cyanide inhibited glucose metabolism. J Phar Exp Ther 189:235-243, 1974.

Isom GE, Burrows GE, Way JL: Effect of oxygen on the antagonism of cyanide intoxication-cytochrome oxidase, in vivo. Toxicol Appl Pharm 65:250-256, 1982.

Ivanov KP: The effect of elevated oxygen pressure on animals poisoned with potassium cyanide. Phar Toxicol 22:476-479, 1959.

Ivankovich AD, Braverman B: Cyanide antidotes and methods of their administration in dogs: a comparative study. Anesthesiology 52:210-216, 1980.

Keilin D: Cytochrome and respiratory enzymes. Proc R Soc Lon (Biol) 104:206-252, 1929.

Kindwall EP: Carbon monoxide and cyanide poisoning, in: Davis JC, Hunt TK (eds): Hyperbaric Oxygen Therapy. Bethesda: Undersea Medical Society, 1977, pp 177-190.

Krapez, JR, Vesey CJ: Effects of cyanide antidotes used with sodium nitroprusside infusions: sodium thiosulfate and Hydroxocobalamin given prophylactically to dogs. Br J Anesth 53:793-804, 1981.

Litovitz TI, Larin RF, Myers RAM: Cyanide poisoning treated with hyperbaric oxygen. Am J Emer Med 1:94-101, 1983. Litovitz TL, Larkin RF, Myers RA: Cyanide poisoning treated with hyperbaric oxygen. Am J Emerg Med 1:94-101, 1983.

Mohler SR: Air crash survival: Injuries and evacuation toxic hazards. Avia Space Environ Med 46:86-88, 1975.

Myers, RAM: Cyanide poisoning (acute) in Myers, RAM (ed): Hyperbaric Oxygen Therapy: A Committee Report, revised. Bethesda: Undersea and Hyperbaric Medical Society 1986, p 40.

Norris JC, Moore SJ, Hume AS: Synergistic lethality induced by the combination of carbon monoxide and cyanide. Toxicology 40: 121-129, 1986.

Sheehy M, Way JL: Effect of oxygen on cyanide intoxication. III. Mithrodate. J Phar Exp Ther 161:163-168,.

Skene, WG, Norman JN: Effect of hyperbaric oxygen in cyanide poisoning, in: Brown IW, Cox B (eds): Proceedings of the Third International Congress on Hyperbaric Medicine. Washington, D.C.: National Academy of Sciences-National Research Council, 1966, pp 705-710.

Symington IS: Cyanide exposures in fires. Lancet 2:91-92, 1978.

Takano N, Myazaki Y: Effect of hyperbaric oxygen on cyanide intoxication: in situ changes in intracellular oxidation reduction. Undersea Biomed Res 7(3):191-197, 1980.

Terrill JB, Montgomery RR: Toxic gases from fires. Science 200:1343-1347, 1978.

Trapp WG: Massive cyanide poisoning with recovery: a boxing day story. Can Med Assn J 120:517, 1970.

Trapp WG, Lepawsky M: One hundred percent survival in five life threatening cyanide poisoning victims treated by a therapeutic spectrum including hyperbaric oxygen. Eighth Annual Conference on Clinical Applications of Hyperbaric Oxygen. Long Beach: Memorial Hospital Medical Center, 1983.

Vogel SN, Sultan TR: Cyanide poisoning, Clin Toxicol 18:367-383, 1981.

Warburg O: Uber die wikung von kohlenoxyd und stick-oxyd auf atmung und garung. Biochem Z 189:354-380, 1927. Way JL, Gibbon Sl: Effect of oxygen on cyanide intoxication. I. Prophylactic protection. J Phar Exp Ther 153:381-385, 1966.

Wetherell HR: The occurrence of cyanide in the blood of fire victims. J Forensic Sci 11:167-173, 1966.

Acute Peripheral Arterial Insufficiency
Acute peripheral arterial insufficiency covers a spectrum of disease that includes acute traumatic and non-traumatic peripheral arterial insufficiency and acute crush injuries (with or without compartment syndrome). Crush or degloving injuries (stripping of the skin and underlying -tissue from the bones, usually of the hands or feet as occurs in wringer or industrial roller injuries) can interrupt large vessels and the continuity of capillary beds. The edema that follows often creates a vicious circle, causing complications such as compartment syndrome (a condition in which pressure within a confined space results in tissue ischemia and resulting dysfunction) and frank sloughing of compromised tissue. Large vessels must be repaired surgically, but the ischemic anoxia resulting from decreased capillary flow may benefit from HBOT, which preserves intracellular levels of ATP, reduces edema, and prevents -reperfusion injury. HBOT also reduces the tendency of WBCs to adhere to the endothelium of injured tissue (believed to be important in secondary ischemia). In a globally hypoxic limb, edema formation can be reduced by 50% if HBOT is initiated within about 8 hours, providing that large vessels have not been disrupted.

The first physiologic effect of hyperbaric oxygen therapy (HBOT) is hyperoxygenation of the tissues affected by acute arterial insufficiency. The effect is not linear but logarithmic, and enough oxygen is physically dissolved in plasma at usual treatment pressures to raise arterial PO2 by a factor of 10 to 15. Because of this increase, the oxygen diffusion distance from capillary to tissue increases three to four times.

Hyperbaric oxygen also causes a vasoconstriction due to the effect of high arterial oxygen tensions in chemoreceptors. This 20 percent reduction in blood flow reduces capillary leakage and diapedesis, thereby reducing edema. HBOT offers a direct antibacterial effect on certain anaerobes, and maintains the killing ability of leukocytes after phagocytosis. HBOT also raises tissue oxygen tension above the level necessary for fibroblasts to lay down collagen, for angiogenesis to occur, and for cellular growth to be supported in healing. Additionally, HBOT increases the effectiveness of the antibiotics that require active transport across the cell wall.

Hyperbaric oxygen theoretically protects tissues from reperfusion injury. HBOT confers this effect either by maintaining the cell's ability to produce scavengers that detoxify free radicals or by preventing lipid peroxidation in cell membranes.

Acute peripheral arterial insufficiency is defined as the traumatic or atraumatic reduction of arterial or arteriolar blood flow to a tissue other than the central nervous system. The mechanisms of injury can be iatrogenic ("trash foot"), traumatic damaging of the artery, or vascular occlusion from a clot or reperfusion injury. The result is acute hypoxia of the ischemic tissues with cellular death. In an area where no blood flow exists, tissue death is inevitable; but in those areas with some perfusion, the use of HBOT maximizes the oxygen content of the serum phase of the blood and can save the threatened tissues. HBOT elevates serum PO2 up to 2000 percent. HBOT has been shown to provide sufficient oxygen delivery to sustain life in a large mammal that has no hematocytes.

The effectiveness of hyperbaric oxygen in clinical human studies is well documented, with acute ischemias arising from surgery and trauma having been particularly well studied. HBOT not only increases the tissue oxygenation, but through an unknown mechanism, enables cells to better tolerate ischemia. However, because HBOT requires adequate circulation to be effective, documentation of blood flow to the affected area should be required if this condition is treated with HBOT. The best currently available technology for indicating the potential usefulness of HBOT in most ischemic areas is transcutaneous oxygen monitoring.

A prospective, randomized, placebo-controlled human study has shown a statistically significant decrease in the necessity for repeat surgery or amputation with use of HBOT.

References

Boerema I, Meijne NG, Brummelkamp WH et al.: Life without blood: a study in the influence of high atmospheric pressure and hypothermia on dilution of blood. J Cardiovasc Surg 133-146, 1960.

Bowersox JC, Strauss MB, Hart GB: Clinical experiences with hyperbaric oxygen therapy in the salvage of ischemic skin grafts and flaps. J Hyperbaric Med. 1:141-149, 1986.

Hill RK, Bright DE, Neubauer RA: Use of hyperbaric in the reanastomosis of the severed ear: a review. J Hyberb Med 163-175, 1990.

Hunt TK, Linsey M, Grislis G, et al.: The effect of varying ambient oxygen tension on wound infection. Ann Surg 181:35-39, 1975.

Hunt TK, Pai MP: The effect of varying ambient oxygen tensions on wound metabolism and collagen synthesis. Surg Gynecol Obstet 135:561-567, 1972.

Hunt TK: Oxygen and Healing. Am J Surg 118:521-525, 1969.

Hunt TK, van Winkle W Jr: Wound healing normal repair, in: Dunphy JE (ed): Fundamentals of Wound Management in Surgery. South Plainfield: Chirurgecom, 1976, pp 1-68.

Kihara M, McManis PG, Schmelzer JD, et al.: Experimental ischemic neuropathy: salvage with hyperbaric oxygenation. Ann Neurol 89-94, 1995.

Nemiroff PM, Merwin GE, Brant T et al.: HBO and irradiation on experimental skin flaps in rats. Surg Forum 549-550, 1984.

Nylander G, Lewis D, Lewis D, Nordström H, Larsson J: Reduction of postischemic edema with hyperbaric oxygen. Plastic Reconstr Surg 76:596-601, 1985.

Perrins DJ: The effect of hyperbaric oxygen on ischemic skin flaps, in: Grabb WC, Myers MB (eds): Skin Flaps. Boston: Little Brown & Co., 1975, pp 53-63.

Sheffield PJ: Tissue oxygen measurements with respect to soft-tissue wound healing with normobaric and hyperbaric oxygen. Hyperb Oxygen Review 18-46, 1985.

Shupak A, Gozal D, Ariel A, Melamed Y, Katz A: Hyperbaric oxygenation in acute peripheral post traumatic ischemia. J Hyperbaric Med 2:7-14, 1987.

Strauss MB, Hargens AR, Gershuni DH, et al.: Reduction of skeletal muscle necrosis using intermittent hyperbaric oxygen in a model compartment syndrome. J Bone Joint Surg 65A:656-662, 1983.

Strauss MB, Hargens AR, Gershuni DH, Hart GB, Akeson WH: Delayed use of hyperbaric oxygen for treatment of a model anterior compartment syndrome. J Orthop Res 4:108-111, 1986.

Strauss MB, Hart GB: Cost-effective issues in hyperbaric oxygen therapy for complicated fractures. J Hyperbaric Med 3:199-205, 1988.

Strauss MB, Hart GB: Hyperbaric oxygen and the skeletal muscle compartment syndrome. Cont Orthopedics 18:167-174, 1989. Undersea and Hyperbaric Medical Society: Hyperbaric Oxygen Therapy. A Committee Report. Bethesda:, UHMS, 1992.

Zamboni WA, Roth AC, Russell RC: Morphologic analysis of the microcirculation during reperfusion of ischemic skeletal muscle and the effect of hyperbaric oxygen. Plast and Reconstr Surg 1110-1123, 1993.

Intravascular Gas Embolism

Air embolism occurs in divers or is secondary to entry of air during vascular surgery, IV therapy, lung biopsy, pulmonary overinflation during mechanical ventilation (usually in children), renal dialysis, angiography, etc.

Intravascular gas embolism (IGE) and its subset, arterial gas embolism (AGE), can occur following exposure to any barometric pressure and may manifest without compression or decompression from one barometric pressure to another. Even in normobaric environments, both traumatic and iatrogenic injury can cause IGE/AGE.

Trauma Causing IGE/AGE

1.Penetrating injury to the heart or major vessels.

2. Blunt injury to the chest with closed epiglottis

Iatrogenic Injury Causing IGE/AGE

1. Pulmonary over pressurization by positive ventilation of a patient or diving barotrauma.

2. Slippage of air into a vein or artery by surgical procedure or catheterization.

3. Insufflation by gas of body cavity or organ cavity:

Pneumoencephalogram

Endometrial/fallopian insufflation

Bowel, bladder, vaginal, or peritoneal cavity insufflation

Gaseous emission from laser vapor

All tissues, including bone, are susceptible to IGE/AGE. In fact, IGE/AGE may involve the spinal cord or the brain. IGE/AGE can produce a spectrum of injury ranging from a transient ischemic attack-like event (TIA), to a major stroke. (A small stroke can also occur.) When the involvement includes the nervous system or heart, a potential life threatening condition exists. The spectrum of IGE/AGE symptomatology extends from simple malaise to full neurologic and cardiovascular collapse.

Gas emboli found in IGE/AGE may impede blood and lymphatic flow by partially or completely obstructing the vessel lumen. The gas emboli result in damage to the vascular endothelial lining which elicits an immune response and a decreased or obstructed blood supply which triggers an ischemic response. Like decompression illness, separated gas within the blood can stimulate a procoagulative state and trigger an inflammatory response. Even if gas emboli resolve, either spontaneously or as a result of hyperbaric oxygen treatment, reperfusion injury in the affected area will likely occur.

Two types of tissue become important during recovery from CNS IGE/AGE. The umbra, is a region of ischemically destroyed or infarcted tissue and is surrounded by the penumbra, a region of viable yet functionally impaired tissue. Acutely, the penumbra may be underperfused and susceptible to conversion to umbra due to a lack of oxygen or energy. Penumbral regions of a CNS injury have been found to fill with polymorphonuclear leukocytes and macrophages. In the early post IGE/AGE period, extravasated leukocytes in an ischemic neurologic tissue function as an oxygen sink. The goal of hyperbaric oxygen therapy is to minimize conversion of penumbral to umbral tissue in regions of marginal brain or spinal cord oxygenation. Hyperbaric oxygen therapy may also prevent leukocyte adherence and truncate lipid peroxidation in the injured region and attenuate the progression of ischemic injury and possible penumbral conversion to umbra.

IGE/AGE exists in three phases, acute (0 to 15 days), subacute (16 days to six months), and chronic (greater than six months). The acute recovery period may include an early phase covering the first six hours after embolic occlusion, during which the penumbral regions are at greatest risk of conversion to umbral regions. If these regions survive longer than six hours, they usually revert to "ex-penumbra" regions. Hyperbaric oxygen therapy may immunomodulate the "ex-penumbra" and speed the recovery to normal neurologic tissue. Further understanding of the mechanisms of IGE/AGE neurologic injury and recovery may lead to current treatment modifications or new treatment modalities. Thus far, the use of pharmacologic agents have been disappointing in IGE/AGE patients. Drugs have failed to ameliorate acute, subacute and chronic neurologic IGE/AGE injury, and recompression is the only successful therapy. Some investigators have shown encouraging clinical results, in patients with residual neurologic damage treated with a series of "tailing" low-dose hyperbaric oxygen treatments (1.5 to 2.5).

Venous gas embolism poses a greater threat to life than AGE only when larger quantities of gas are involved. Venous gas microembolism is often equated with decompression illness. Subclinical venous gas microembolism may be a part of every decompression. For repetitive air dives, decompression from most allowable bottom times may produce pulmonary arterial bubbles detectable with Doppler evaluation.

A patent foramen ovale is present in approximately 34 percent of the adult population. A patent foramen ovale would allow a venous bubble to cross into the arterial circulation. Over pressurization of the pulmonary artery may temporarily pneumatically block the pulmonary vasculature and allow build up of intravascular gas emboli in the precapillary bed. A sudden release of the high pressures would allow intravascular emboli to cross the pulmonary vascular filter.

References

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Van Meter K, Harch P, Weiss L: 14 year experience of the use of a tailing of hyperbaric oxygen treatments to lessen or resolve neurologic residual injury in arterial gas embolism (AGE) or decompression illness (DCI) in the acute 0-15 day and sub-acute 16 day to 6 month post-injury period. Proceedings of the 1995 Gulf Coast Chapter of the UHMS. New Orleans: UHMS, 1995. (in press).

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Warren LP, Djang WT, Moon RE: Neuro imaging of diving injuries to the central nervous system. Am J Neuroradiol 9:933-938, 1988.

Warren RB, Philip RB, Inwood MJ: The ultrastructural morphology of air embolism platelet adhesion to the interface and endothelial damage. Br J Exp Path 54:163-172, 1973.

Yeakel AE. Lethal air embolism from plastic blood-storage container. J Am Med Assn 204(3):175-177, 1968.

Zamboni WA, Roth AC, Russel RC: Morphologic analysis of the microcirculation during reperfusion of ischemic skeletal muscle and the effect of hyperbaric oxygen. Plast Reconstr Surg 91:1110-1123, 1993.

Carbon Monoxide Poisoning
Carbon monoxide (CO) remains among the most common poisons in the industrialized world and a leading cause of poison-related deaths. A survey of death certificate reports in the United States for a 10 year period ending in 1988 indicated that CO exposure contributed to the deaths of more than 56,000 people. Automotive exhaust, home heating, and industrial exposure are the most common sources. Fumes from paint strippers containing methylene chloride are metabolized to carbon monoxide (CO) in the body and can cause severe poisoning. Flu-like symptoms may occurs without fever. Headache, nausea, vomiting, weakness, and collapse often are followed by coma and death. The diagnosis cannot be made unless exposure is suspected. The skin is cherry red after death; however, this is not seen clinically. The percentage of carboxyhemoglobin (COHb)in the blood does not correlate with the prognosis and often does not correspond to the clinical condition caused by tissue toxicity resulting from disruption of cellular cytochrome metabolism and initiation of lipid peroxidation. HBOT is indicated in the presence of almost any sign or symptom (even if the patient looks well). The sooner HBOT is initiated, the better. The mortality rate in severe cases is 13.5% when HBO is initiated < 6 hours and 30.1% when initiated > 6 hours after rescue.

Neurological and psychiatric abnormalities also occur in delayed fashion after patients are acutely treated for CO poisoning and, seemingly, have recovered. These delayed neurological sequelae (DNS) occur from two to 40 days after CO exposure. Manifestations of DNS include disorientation, apathy, bradykinesia, gait disturbances, aphasia, apraxia, incontinence, personality changes, and rarely, seizures and coma. The incidence of DNS was 35.8 percent for those patients treated with either ambient pressure oxygen or with HBOT at greater than six hours. In contrast, the incidence of DNS among patients treated with HBOT in less than six hours was 7 percent.

The physiological benefits of hyperbaric oxygen therapy (HBOT) are: improvement of oxygenation and hastened COHb dissociation, restoration of mitochondrial function, and inhibition of adherence of leukocytes to the microvascular endothelium.

References

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Koren G, Sharav T, Pastuszak A, Garrettson LK, Hill K, Samson I, et al.: A multicenter, prospective study of fetal outcome following accidental carbon monoxide poisoning in pregnancy. Reprod Toxicol 5:397-403, 1991.

Krantz T, Thisted B, Strom J, Sorensen MB: Acute carbon monoxide poisoning. Acta Anaesthesiol Scand 32:278-282, 1988. Lamy M, Hauguet M: Fifty patients with carbon monoxide intoxication treated with hyperbaric oxygen therapy. Acta Anes Belgica 1:49-53, 1969.

Mathieu D, Nolf M, Durocher A: Acute carbon monoxide poisoning: risk of late sequelae and treatment by hyperbaric oxygen. Clin Toxicol 23:315-324, 1985.

Mayevsky A, Meilin S, Rogatsky GG, Zarchin N, Thom SR: Multiparametric monitoring of the awake brain exposed to carbon monoxide. J Appl Physiol (in press).

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Raphael, JC, Elkharrat D, Jars-Guincestre MC, Chastang C, et al.: Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication. Lancet 19:414-419, 1989.

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Silverman CS, Brenner J, Murtagh FR: Hemorrhagic necrosis and vascular injury in carbon monoxide poisoning: MR demonstration. AJNR 14:168-170, 1993.

Smith JS, Brandon S: Morbidity from acute carbon monoxide poisoning at three-year follow-up. Br Med J 1:318-321, 1973.

Thom SR: Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats. Toxicol Appl Pharmacol 123:248-256, 1993.

Thom SR: Leukocytes in carbon monoxide-mediated brain oxidative injury. Toxicol Appl Pharmacol 123:234-247, 1993.

Thom SR, Mendiguren I, Nebolon M, Campbell D, Kilpatrick L: Temporary inhibition of human neutrophil B2 integrin function by hyperbaric oxygen (HBO). Clin Res 42:130A, 1994.

Thom SR, Ischiropoulos H: Nitric oxide released by platelets inhibits neutrophil B2 integrin function following acute carbon monoxide poisoning. Toxicol Appl Pharmacol 128:105-110, 1994.

Thom SR, Taber RL, Mendiguren II, Clark JM, Hardy KR, Fisher AB: Delayed neuropsychological sequelae following carbon monoxide poisoning and its prophylaxis by treatment with hyperbaric oxygen. Ann Emer Med 25:474-480, 1995.

Tomaszewski C, Rudy J, Wathen J, Brent J, Rosenberg N: Prevention of neurologic sequelae from carbon monoxide by hyperbaric oxygen in rats. Ann Emer. Med 21:631-632, 1992.

VanHoesen KB, Camporesi EM, Moon RE, Hage ML, Piantadosi, CA: Should hyperbaric oxygen be used to treat the pregnant patient for acute carbon monoxide poisoning. JAMA 261:1039-1043, 1989.

Zhang J, Piantadosi CA: Mitochondrial oxidative stress after carbon monoxide hypoxia in the rat brain. J Clin Invest 90:1193-1199, 1991.

Clostridial Myonecrosis (Gas Gangrene)

Clostridium perfringens is the most common cause of gas gangrene, -although one or more other anaerobic organisms are usually present. The syndrome is primarily mediated by a toxin, lecithinase, which lyses Red Blood Cells (RBCs) and severely damages muscle, cell membranes, and the kidney. Profound shock that responds only to whole blood or packed RBCs can occur. Death may ensue within 6 hours of diagnosis unless immediate treatment is given. The prognosis is especially grave in an elderly compromised host who has gangrene of the abdomen or trunk. The usefulness of HBOT in gas gangrene has been demonstrated in good animal studies and large clinical series. If used, HBOT must be carried out early in the course of the disease before surgical debridement. Surgery requiring general anesthesia should generally be deferred until after the first 2 or 3 HBOT treatments are given, because surgery entails a delay in HBOT, and further spread of the infection and systemic toxicity may ensue. Furthermore, the demarcation between viable and necrotic tissue is clearer after 2 HBOT treatments, often making possible less disfiguring surgery and salvage of entire limbs. . Risk of death in a patient with truncal gangrene is 75% if HBOT is -initiated > 24 hours after diagnosis and < 18% if initiated within 24 hours. When a limb is involved, the mortality rate may be > 9% if HBOT is delayed > 24 hours, but it approaches zero if initiated in <24 hours, regardless of the type or time of surgery.

The action of hyperbaric oxygen on Clostridia (and other anaerobes) is based on the formation of oxygen free radicals in the absence of free radical degrading enzymes, such as superoxide dismutases, catalases, and peroxidases.

References

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Brummelkamp WH: Considerations on hyperbaric oxygen therapy at three atmospheres absolute for clostridial infections type welchii. Ann NY Acad Sci 117:688-699, 1965.

Darke SG, King AM, Slack WK: Gas gangrene and related infection: classification, clinical features and aetiology, management and mortality. A report of 88 cases. Br J Surg 64:104, 1977.

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Demello FJ, Haglin JJ, Hitchcock CR: Comparative study of experimental Clostridium perfringens infection in dogs treated with antibiotics, surgery and hyperbaric oxygen. Surgery 73:936-941, 1973.

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Maudsley RH: Proceedings: post-operative gas gangrene managed by hyperbaric oxygen. J Bone Jt Surg Br 57:251, 1975.

Nier H, Kremer K: Der Gasbrand-weiterhin ein diagnostisches und therapeutisches problem. Zentrabl Chir 109;402-417, 1984.

Nier H, Sailer R, Palomba P: Hyperbaric oxygen treatment in gas gangrene. Dtsch Med Wochenschr 103:1958, 1978

Nora PF, Mousavipour M, Laufman H: Mechanisms of action of high pressure oxygen in Clostridium perfringens exotoxin toxicity, in: Brown IW, Cox BG (eds): Hyperbaric Medicine, Publ. No. 1404. Washington DC: National Academy of Sciences, National Research Council 1966, pp 544-51.

Nora PF, Mousavipour M, Mittlepunkt A, Rosenburg M, Laufman H: Brain as target organ in Clostridium perfringens cytotoxin. Arch Surg 92:243-246, 1966.

Pailler JL, Labeau F: La gangrene gazeuse: Une affection militaire? Acta Chir Belg 86:63-71, 1986.

Peirce EC II: Gas gangrene. A critique of therapy. Surg Rounds 1984; 7:17-25.

Roding B, Groenveld PHA, Boerema I: Ten years of experience in the treatment of gas gangrene with hyperbaric oxygen. Surg Gynecol Obstet 134:579, 1972.

Sailer R, Junemann A, Ghazwinian R: Therapy of gas gangrene. Comparison of results of standard and hyperbaric oxygen therapy. Med Kin 69:1620, 1974.

Schoemaker G: Oxygen tension measurements under hyperbaric conditions, in: Boerema, Brummelkamp WH, Meijne NG (eds). Clinical application of hyperbaric oxygen. Amsterdam: Elsevier, 1964, pp 330-335.

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Slack WK, Hanson GC, Chew HE: Hyperbaric oxygen in the treatment of gas gangrene clostridial infection. A report of 40 patients treated in a single-person hyperbaric oxygen chamber. Br J Surg 56:505, 1969.

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Compromised Skin
Grafts and Flaps: Reconstructive Work
Skin grafts and compromised skin flaps represent a classical problem involving insufficient oxygen supply to tissue. Plastic surgeons use the grafts and flaps to repair serious damage, and to close or cover wounds. In creating skin grafts or flaps, a strip of skin is sharply removed from all or part of its adjacent tissues. The surgery removes all of the blood supply from the skin graft, and eradicates much of the blood supply in the skin flap.

Skin grafts are especially susceptible to hypoxic injury. Once a graft is in place, the bed and the edges of the graft site provide the only sustenance available until neovascularization occurs. Hyperbaric oxygen therapy (HBOT) maximizes oxygen transfer for these sites. HBOT ameliorates vascular problems triggered by hypoxia. Three of the primary effects of HBOT, hyperoxygenation, edema reduction, and neovascularization, prove particularly useful to surgeons and plastic surgeons.

Providing hyperoxgenation increases the oxygen tension in the graft bed and wound margins up to 1500 percent. In turn, the hyperoxygenation causes a marked increase in the effectiveness of the blood or plasma that reaches the graft through compromised blood vessels. The volume of tissue that derives sufficient oxygen from a single damaged blood vessel increases 16 fold, and marked tissue salvage results. This same effect maximizes the rate new blood vessels mature at the site where the graft ultimately attaches.

Hyperbaric techniques also offer strategies for reducing edema. The edema reduction effect, induced by the relative spasm of a precapillary arteriolar sphincter, helps to limit the swelling of the graft or flap. In addition, an increase in the mean diffusion radii occurs, resulting in the amount of tissue being supplied with oxygen increasing significantly. The high oxygen tensions achievable with HBOT induce large oxygen gradients, increasing macrophage migration, proline synthesis, and neovascularization. Once this neovascularization occurs, the beneficial effects of HBOT for organs begins. Among other things, fluids begin to flow to tissues and organs more readily, limiting damage from reperfusion injury.

Skin grafts, by their very nature, hypoxic. Grafts are used to cover areas that are devoid of skin due to trauma or disease, so the recipient site is ischemic, and it is this site that will provide the support for the graft. The skin graft is cut from all of its blood supply. Next, it is placed upon the compromised tissue base, where it must initially rely completely upon oxygen that diffuses from the base, and later upon rapid angiogenesis from the base and wound margins so that the graft's vascular structure can be reconstructed. Skin flaps must overcome similar problems due to the stretching and twisting of their vascular tree.

HBOT ameliorates the hypoxia, post-operative swelling, and ischemia of grafts and flaps. HBOT provides high concentrations of oxygen to the graft bed so that more oxygen can diffuse into the graft to sustain it during an ischemic period. The anti-edema effect of HBOT improves tissue oxygenation by reducing the distance oxygen must diffuse, and by improving perfusion.

The benefit of HBOT for the preparation of a base for skin grafting and the preservation of compromised skin grafts has been well documented as effective.

References

Bowersox JCC, Strauss MB, Hart GB: Clinical experience with hyperbaric oxygen therapy in the salvage of ischemic skin flaps and grafts. J Hyperbaric Medicine 1:141-149, 1986.

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Davis JC, Hunt, TK: Hyperbaric Oxygen Therapy. Bethesda: Undersea and Hyperbaric Medical Society, 1977, pp 229-238.

Fisher B, Jian KK, Braun E, Lehri S: Handbook of Hyperbaric Oxygen Therapy. Berlin: Springer-Verlag, 1988, pp 109-111.

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Gruber RP, Brinkley FB, Amato JJ, et al.: Hyperbaric oxygen and pedicle flaps, skin grafts, and burns. Plast Reconstr Surg 24-30, 1970.

Hill RK, Bright DE, Neubauer RA: Use of hyperbaric oxygen in the reanastomosis of the severed ear: a review. J Hyperbaric Medicine 4(4):163-175, 1990.

Hunt TK, van Winkle W Jr.: Wound healing normal repair, in Dunphy JE (ed): Fundamentals of Wound Management in Surgery. South Plainfield: Chirurgecom, 1976, 1-68.

Hunt TK., Pai MP: The effect of varying ambient oxygen tensions on wound metabolism and collagen synthesis. Surg Gynecol Obstet 561-567, 1972.

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Nemiroff PM, Merwin, GE, Brant T, Cassisi NJ: HBO and irradiation on experimental skin flaps in rats. Surg Forum 35:549-550, 1984.

Nylander G, Lewis D, Nordstrom H, Larsson J: Reduction of postischemic edema with hyperbaric oxygen. Plast Reconst Surg 596-601, 1985.

Perrins DJD, Cantab MB: Influence of hyperbaric oxygen on the survival of split thickness skin grafts. Lancet 1:868-871, 1967.

Perrin DJD: Influence of hyperbaric oxygen on the survival of split thickness skin grafts. Lancet 868-871, 1967.

Perrins DJD: The effect of hyperbaric oxygen on ischemic skin flaps, in: Grabb WC, Myers MB (eds): Skin Flaps. Boston: Little Brown & Co., 1975, 53-63.

Reedy MK, Capen CV, Bakker DP, et al.: Hyperbaric oxygen therapy following radical vulvectomy: an adjunctive therapy to improve wound healing. Gynecologic Surg 13-16, 1994.

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Zamboni WA, Roth AC, Russell RC, Nemiroff PM, et al.: The effect of acute hyperbaric oxygen therapy on axial pattern skin flap survival when administered during and after total ischemia. J Reconstr Micros 5:343-347, 1989.

Zamboni WA: Hyperbaric oxygen reduces ischemia-induced skeletal muscle injury. Plast Recontr Surg 609-609, 1996.

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. Plast and Reconstr Surg 1110-1123, 1993.

Decompression Illness

Decompression illness (DCI) is an affliction of gas separation causing bubbles (foreign bodies) in the tissues and blood resulting from a decrease in ambient pressure. The gas separation results in a number of responses ranging from an immune "foreign body" response, ischemia, and finally a reperfusion injury. The separation of gas, to form bubbles in the blood or tissue, impedes blood and lymphatic flow by direct mechanical obstruction, as well as directly disrupts or distorts tissues when intratissue bubble formation occurs. Intravascular gas perturbs the vessel.s endothelial surface and the cell surfaces of the platelets and white blood cells. Should recompression relieve the bubble(s), a reperfusion injury in the affected area will likely occur.

Often, intravascular gas embolism (IGE) complicates DCI and may result from either a variant of DCI or a complication arising from separate, concurrent pulmonary barotrauma with gas embolization. Intravascular gas embolic occlusion potentially blocks off-gassing tissue areas during decompression and may potentiate the local DCI injury in the involved area.

All tissues, including bone, are susceptible to DCI. When the involvement includes the nervous system or heart, a potential life threatening condition exists. The spectrum of DCI symptomatology extends from simple malaise to full cardiovascular collapse. Central nervous system (CNS) injury may be subtle or blatant and peripheral nerves may be involved. DCI may also present as a variant of the systemic inflammatory response syndrome.

DCI has classically been categorized into Type I and Type II (and recently Type III when the injury occurs concurrent with and is complicated by intravascular gas embolism. Type I involves joints and their ligaments, lymphatics, and skin. Type II involves the central nervous system (brain and spinal cord, autonomic nervous system, and peripheral nervous system), the lungs (chokes), and the cardiovascular system.

Recompression treatment in acute DCI has three main effects bubble compression, aerobic support for ischemic tissues, and an anti-inflammatory effect. Recompression causes reduction of the size of bubbles in tissues and in vessels in accordance with the ideal gas law. Besides shrinking the bubbles mechanically to improve liquid flow, their resulting smaller size forces them back into solution. Recompression provides aerobic support by filling the plasma fraction of blood with an increased content of dissolved oxygen to support the oxygen needs of downstream tissues. This also promotes the diffusion of the inert gas out of the separated gas phase bubble, and facilitates the blockade of potential inflammatory mediators. Hyperbaric oxygen therapy blunts leukocyte adhesion and blocks lipid peroxidation. Thus, hyperbaric oxygen therapy recompression allows dissolution of the separated gas and attenuates the inflammatory response which occurs during reperfusion of acutely injured ischemic tissue.

DCI may involve the spinal cord or the brain. DCI can produce a spectrum of injury ranging from a transient ischemic attack-like event (TIA), a small stroke, or a major stroke. CNS ischemia produces two zones of injury. The umbra, is a region of ischemically destroyed or infarcted tissue and is surrounded by the penumbra, a region of viable, yet functionally impaired tissue. Penumbral regions of a CNS injury have been found to fill with polymorphonuclear leukocytes (PMN's) and macrophages. In the early post DCI period, extravasated leukocytes in an ischemic CNS tissue function as an oxygen sink. The goal of hyperbaric oxygen therapy is to minimize conversion of penumbral to umbral tissue in regions of marginal oxygenation in the brain or spinal cord.

The DCI injury involves acute, subacute, and chronic phases. Further understanding of the immune/ inflammatory processes may lead to modifications of current treatments or new treatment modalities. Thus far, the use of pharmacologic agents has been disappointing in DCI patients. Drugs have failed to ameliorate acute, subacute, and chronic neurologic DCI injury. Recompression is the only effective treatment of this devastating disease.

Lymphocytes can be immunomodulated by different oxygen tensions. Subacutely and chronically they may roam the penumbra much as they would in a healing wound. If perfusion of the penumbra is not re-established, then dysfunctional regions of poorly perfused neuronal tissue may never again become functional. Successful reperfusion modulated by lymphocytes, macrophages and fibroblasts may account for the accelerated recovery in neurologically injured DCI patients undergoing a "tailing" series of hyperbaric oxygen treatments. New capillary growth in the ground substance matrix can be accelerated in ischemically injured CNS tissue undergoing hyperbaric oxygen therapy. However, the gradual recovery in a few patients with untreated severe neurological injuries from DCI was observed at the turn of the century.

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Osteoradionecrosis
The recent introduction of radiation therapy for the treatment of solid tumors allows previously untreatable cancers to be cured. Now physicians face the challenge of aiding survivors. Unfortunately, the radiation beam used to fight cancer damages more than the tumor. Normal tissue in the path of the beam often sustains damage. Destruction of tissue also occurs. Even today, many physicians consider chronic radiation effects as irreversible, but hyperbaric oxygen therapy (HBOT) offers opportunities to repair damage.

Both bone and soft tissue suffer damage from therapeutic radiation. Bone is 1.8 times as dense as soft tissue and thereby absorbs a proportionately larger dose of incident radiation than does soft tissue.

High doses of radiation cause a proliferative endarteritis causing ischemia, and eventually death of bone in the distribution of the involved blood supply. Additionally, radiation upsets the normal balance of osteoclastic destruction and osteoblastic reconstruction occurring in bone. Cell death of these osteocytes and osteoblasts leads to osteoporosis and eventually to osteonecrosis.

Clinically significant osteonecrosis (ORN) usually develops over a period ranging from four months to several years. There is no satisfactory treatment for radiation necrosis using available conventional means. One barrier to healing involves nutrients providing adequate nutrition and oxygen to radiation devascularized tissue presented a previously insurmountable challenge. Radiation ulcers are painful, and the prolonged use of narcotic analgesics can lead to addiction. High failure rates confront reconstructive surgeons working in irradiated areas, due to problems with healing.

Osteoradionecrosis becomes clinically significant when it develops at four anatomic sites chest wall, mandible, pelvis, vertebral column, and skull. Damage to the ribs and sternum can result following radiation therapy for tumors of the breast, chest wall, or lung. Pathologic fractures in irradiated ribs can result from coughing, or from merely deep breathing.

Irradiation damage to the skull from treatment of orbital or brain tumors is rare, primarily because of the use of highly fractionated doses of radiation, but does occur. The radiotherapy treatment of pelvic neoplasms can lead to radionecrosis of the lumbar vertebrae, femur, or pelvis; pathologic stress fractures can result from injury to these weight-bearing structures. Doses of radiation necessary to produce adequate tumor kill in head and neck cancers are accompanied by an unfortunately high incidence of osteoradionecrosis. The mandible is often involved following radiotherapy of these tumors, and is over represented in osteoradionecrosis.

Osteoradionecrosis most commonly involves the mandible. The mandible is often involved because head and neck cancers are common, and radiation therapy in these cancers is very effective. Most cases of mandibular osteoradionecrosis originate from tooth extraction after development of radiation caries. The trauma of tooth extraction causes a breakdown of gum tissue and subsequent progressive bone necrosis. Exposed bone is often visible. Granulation tissue cannot form a bridge over dead bone, and the infection continues despite meticulous wound care and antibiotics; the resolution rate is only about 8% without HBOT.

Because the clinical and the radiographic pictures fail to match and no laboratory tests or reliable irradiation tissue tolerance curves exist, physicians rely on a simple working definition of osteoradionecrosis. Any exposed bone in a field of irradiation failing to heal after a trial of conservative treatment earns the ORN label. So does the presence of radiographically demonstrated osteoradionecrosis.

Beginning in 1979, Marx and others demonstrated that osteoradionecrosis is a wound healing defect related to a chronic hypoxic state. In 1984, Marx published a study of 150 cases of osteoradionecrosis in the mandible. In his examination, Marx divided the disease into three stages of advancing clinical activity. This staging and the HBOT treatment of osteoradionecrosis he described became the standard for planning the treatment of mandibular and soft tissue ORN. The strategy has implications for the treatment of ORN in other tissues as well.

The 1990 Consensus Paper of the National Cancer Institute on the Oral Complications of Cancer therapies states "The treatment of ORN with antibiotics and surgical debridement frequently fails, with progressive involvement of the remaining mandible. The keystone of the treatment of ORN is the provision of adequate tissue oxygenation in the damaged bone. This is best done by using hyperbaric oxygen therapy (HBOT). In the event that dental extractions are required following radiation, meticulous surgical technique and antibiotic prophylaxis are necessary."

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Progressive Necrotizing Infection (Meleney's ulcer)

The term "Meleney's ulcer" describes a distinct pathological entity also called progressive bacterial synergistic gangrene.

The diagnostic criteria for Meleney's ulcer, as described in the literature, would include (1) a slowly progressive, superficial necrotizing process; (2) evidence of a variety of micro-areophilic, anaerobic, facultative, or amoebic organisms; (3) hypoxic wound environment, and (4) microvascular thrombosis in a full thickness ulcer.

Some diabetic foot ulcerations may meet the criteria for designation as a Meleney's ulcer. All diabetic ulcerations are not automatically Meleney's ulcers. Although all diabetic ulcer wounds are hypoxic and have microvascular thrombosis, a particular wound must also have an expanding margin, because progressive necrosis is the sine qua non of Meleney's ulcer.

The mechanisms by which HBOT exerts a beneficial effect for Meleney's ulcer treatment are similar to those already described for other necrotizing infections. In the acute phase, HBOT (1) inhibits growth of anaerobic or micro-aerophilic antibiotic organisms, (2) enhances neutrophil function compromised by hypoxia, and (3) increases the efficacy of certain antibiotics (particularly those requiring oxygen dependent intracellular transport). Once spread of the necrotic process has been halted, HBOT may promote healing by stimulating angiogenesis and granulation tissue formation, as in other conditions.

Meleney Ulcer is an old term used as a description of a rare progressive cutaneous infection. Doctors Frank Meleney and George Brewer described this clinical entity in 1926 as a synergistic necrotizing bacterial infection. They defined it as a progressively expanding infection created by the synergism between aerophilic and anaerobic/microaerophilic bacteria. The eponymic term, Meleney Ulcer, is no longer commonly used, and has been supplanted by Progressive Necrotizing Infection.

The utility of hyperbaric oxygen therapy (HBOT) in progressive necrotizing infections is very well established in the medical literature. HBOT is adjunctive to the standard surgical and antibiotic therapy.

References

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Eltorai IM, Hart GB, Strauss MB, Montroy R, Juler GL The role of hyperbaric oxygen in the management of Fournier.s gangrene. Int Surg 7153, 1986.

Grainger RW, MacKenzie DA, McLachlin AD Progressive bacterial synergistic gangrene Chronic undermining ulcer of Meleney. Canad J Surg 10439-444, 1967.

Iorianni P, Oliver GC Synergistic soft tissue infections of the perineum. Dis Colon Rectum 640-644, 1992.

Kingston D, Seal DV Current hypotheses on synergistic microbial gangrene. Br J Surg 77260-264, 1990.

Maisel RH, Karlen R Cervical necrotizing fasciitis. Laryngoscope 795-798, 1994.

Reigels-Nielsen P, Hesselfeldt-Nielson J, Bang-Jensen E, Jacobsen E Fournier's gangrene 5 patients treated with hyperbaric oxygen. J Urol 132918, 1984.

Riseman JA, Zamboni WA, Curtis A, et al. Hyperbaric oxygen therapy for necrotizing fasciitis reduces mortality and the need for debridements. Surgery 108847-850, 1990.

Sandusky WR Frank L. Meleney Pioneer Surgeon-Bacteriologist. Arch Surg 118151-155, 1983.

Shupak A, Greenberg E, Hardoff R et al. Hyperbaric oxygenation for necrotizing (malignant) otitis externa. Arch Otolaryngol Head Neck Surg 1470-1475, 1989.

Spirnak JP, Resnick MI, Hampel N, Persky L Fournier's gangene report of 20 patients. J Urol 131289, 1984.

Zamboni WA, Riseman JA, Kucan JO Management of Fournier.s gangrene and the role of hyperbaric oxygen. J Hyper Med 177-185, 1990.

Burns
The use of hyperbaric oxygen therapy in the treatment of thermal burns began in 1965 when Ikeda and Wada observed more rapid healing of second-degree burns in a group of coal miners who were being treated for carbon monoxide poisoning. Subsequent studies demonstrated that hyperbaric oxygen therapy, when used as an adjunct in a comprehensive program of burn care, can significantly improve morbidity and mortality, reduce length of hospital stay, and lessen the need for surgery. Deep second-degree burns may deteriorate to full-thickness loss, and HBOT may be considered to reduce hypoxia and edema formation by preserving ATP and aerobic glycolysis. HBOT also reduces the fluid requirement by 35% within the first 24 hours. To be most effective, HBOT must be started within 24 hours of the burn, preferably as soon as possible. Additionally, hypertrophic scarring and contracture are reduced. Fluid resuscitation must be continued without interruption while the patient is in the chamber. The patient must also be protected from heat loss. HBOT for serious burns should only be used in a critical care setting.

References

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Arturson G The pathophysiology of severe thermal injury. J Burn Care Rehab 6(2) 129, 1985.

Bleser F, Benichoux R Experimental surgery the treatment of severe burns with hyperbaric oxygen. J Chir (Paris) 106281, 1973.

Boykin JV, Eriksson E, Pittman RN In vivo microcirculation of a scald burn and the progression of post burn dermal ischemia. Plast. Reconstr. Surg 66191, 1980

Brown IW, Cox BG (eds) Proceedings of the Third International Congress on Hyperbaric Medicine, Publ No. 1404. Washington, DC National Academy of Sciences, National Research Council, 1966, pp 611.

Cianci P, Lueders H, Lee H, et al. Adjunctive hyperbaric oxygen reduces the need for surgery in 40-80 percent burns. J. Hyperbar Med 397, 1988.

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Cianci P, Lueders HW, Lee H, et al. Adjunctive hyperbaric oxygen therapy reduces length of hospitalization in thermal burns. J Burn Care Rehabil 10432, 1989.

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Grim P S, Nahum A, Gottlieb L, et al. Lack of measurable oxidative stress during HBOT therapy in burn patients. Undersea Biomed Res Suppl (16)22, 1989.

Grogan JB Altered neutrophil phagocytic function in burn patients. J Trauma 16734, 1976.

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Gruber RAP, Brinkley B, Amato JJ, et al. Hyperbaric oxygen and pedicle flaps, skin grafts, and burns. Plast. Reconstr. Surg 4524, 1970.

Hammarlund C, Svedman C, Svedman P Hyperbaric oxygen treatment of healthy volunteers with UV-irradiated blister wounds. Burns 17296, 1991.

Hart GB, O.Reilly RR, Broussard ND, et al. Treatment of burns with hyperbaric oxygen. Surg Gynecol Obstet 139693, 1974.

Hartwig VJ and Kirste G Experimentele untersuchungen uber die revaskularisierung von verbrennungswunden unter hyperbarer sauerstofftherapie. Zbl Chir 991112, 1974

Heggers JP, Robson, MC, Zachary LS Thromboxane inhibitor for the prevention of progressive dermal ischemia due to the thermal injury. J Burn Care Rehabil 6466, 1980.

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Ikeda K, Ajiki H, Nagao H, et al. Experimental and clinical use of hyperbaric oxygen in burns, in Wada J, Iwa T (eds) Proceedings of the Fourth International Congress on Hyperbaric Medicine. Tokyo Igaku Shoin Ltd., 1970, p 370.

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Ketchum SA, Zubrin JR, Thomas AN, et al. Effect of hyperbaric oxygen on small first, second and third degree burns. Surg Forum 1865, 1967.

Ketchum SA, Thomas AN, Hall AD Angiographic studies of the effect of hyperbaric oxygen on burn wound revascularization, in Wada J and Iwa T (eds) Proceedings of the Fourth International Congress on Hyperbaric Medicine. Tokyo Igaku Shoin Ltd., 1980, p 388.

Korn HN, Wheeler ES, Miller TA Effect of hyperbaric oxygen on second degree burn wound healing. Arch Surg 112732, 1977.

Lamy ML, Hanquet MM Application opportunity for OHP in a general hospital - a two years experience with a monoplace hyperbaric oxygen chamber, in Wada J and Iwa T (eds) Proceedings of the Fourth International Congress on Hyperbaric Medicine (1970). Tokyo Igaku Shoin, Ltd., p 517.

Mader JT, Brown GL, Guckian JC, et al. A mechanism for the amelioration of hyperbaric oxygen of experimental staphylococcal osteomyelitis in rabbits. J Infect Dis 42915, 1980.

Maxwell G, Meites H, Silverstein P Cost effectiveness of hyperbaric oxygen therapy in burn care. Winter Symposium on Baromedicine, Aspen 1991 .

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Niccole MW, Thornton JW, Danet RT, et al. Hyperbaric oxygen in burn management a controlled study. Surgery 82727, 1977.

Niu AKC, Yang C, Lee HC, et al. Burns treated with adjunctive hyperbaric oxygen therapy a comparative study in humans. J Hyperbar Med 275, 1987.

Nylander G, Nordstrom H, Eriksson E Effects of hyperbaric oxygen on oedema formation after a scald burn. Burns 10193, 1984.

Ogle CK, Alexander JW, Nagy E, et al. A long-term study and correlation of lymphocyte and neutrophil function in the patient with burns. J Burn Care Rehab 112105, 1990.

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Ray CS, Green G, Cianci P Hyperbaric oxygen therapy in burn patients cost effective adjuvant therapy (poster presentation). Undersea Biomed Res Suppl 1877, 1991.

Ross JC, Cianci PE Barotitis media resulting from hyperbaric oxygen therapy. a retrospective study of 395 consecutive cases. Undersea Biomed Res Suppl 1702, 1990.

Saunders J, Fritz E, Ko F, et al. The effects of hyperbaric oxygen on dermal ischemia following thermal injury. Proceedings of the American Burn Association (New Orleans), 1989, p 58.

Stewart RJ, Yamaguchi KT, Cianci PE, et al. Effects of hyperbaric oxygen on adenosine triphosphate in thermally injured skin. Surg Forum 3987, 1988.

Stewart RJ, Yamaguchi KT, Cianci PE, et al. Burn wound levels of ATP after exposure to elevated levels of oxygen. Proceedings of the American Burn Association, (New Orleans), 1989, p 67.

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Chronic Refractory Osteomyelitis
Osteomyelitis represents an inflammatory process with a bacterial infection involving bone. The disease involves ischemia as well as infection, and it may be acute, subacute, or chronic. The term "refractory osteomyelitis" refers to failure to heal despite adequate surgical and antibiotic therapy.

Clinicians use hyperbaric oxygen therapy (HBOT) for the treatment of refractory, acute, or chronic osteomyelitis. HBOT is purely adjunctive and must be used with appropriate parenteral antibiotics (best determined by bone culture), surgical debridement, nutritional support, and reconstructive surgery.

In clinical practice, choosing the best treatment for osteomyelitis presents physicians with enormous challenges. Major therapies include antibiotics, surgery, and adjunctive therapies, such as HBOT.

The results of several open clinical trials indicate that adjunctive hyperbaric oxygen therapy is useful in the treatment of chronic osteomyelitis. To avoid the many variables of clinical osteomyelitis and to objectively evaluate the effect of HBOT in the laboratory, Mader used the Staphylococcus aureus osteomyelitis rabbit model developed by Norden. Hyperbaric oxygen alone was as effective as cephalothin in the treatment of experimental S. aureus osteomyelitis.

To establish the mechanism of this effectiveness of hyperbaric oxygen in osteomyelitis, further studies were done. These studies provided evidence for the following conclusions hyperbaric oxygen, when administered under standard treatment conditions, was as effective as cephalothin in the eradication of S. aureus from infected bone; osteomyelitic bone in the experimental model has decreased blood flow and a greatly decreased partial pressure of oxygen; HBOT does not directly affect this strain of S. aureus; and HBOT can restore intramedullary oxygen tensions to physiologic or supraphysiologic levels, but this short exposure does not acutely increase blood flow in osteomyelitic bone. One mechanism for HBOT's effectiveness in S. aureus osteomyelitis may be the increase of intramedullary oxygen to tensions that maximize the efficiency of kill by phagocytes.

Increasing the oxygen tension produces a direct lethal effect on strict anaerobic organisms, and on some micro-aerophilic aerobic organisms. During hyperbaric oxygen therapy, an increase in oxygen tension leads to the increased concentration of superoxide, both intracellularly and extracellularly. Increased superoxide levels predispose to increased hydrogen peroxide production (as well as higher output of other toxic oxygen radicals). Anaerobic organisms are extremely sensitive to these proliferating oxygen radicals because most lack the superoxide-degrading enzyme, superoxide dismutase, and the hydrogen peroxide-degrading enzyme, catalase.

Thus, an increase in the oxygen tension with subsequent oxygen radical formation proves lethal or bacteriostatic for anaerobic organisms. Anaerobic organisms make up approximately 25 percent of the isolates in non-hematogenous osteomyelitis. Hyperbaric oxygen also augments the bactericidal action of the aminoglycoside class of antibiotics. The major antibiotics in this drug class include Gentamicin, Tobramycin, Amikacin, and Netilmicin. The aminoglycosides lack good antibacterial activity under low oxygen tensions. Low oxygen tensions are found in osteomyelitic bone, and adjunctive hyperbaric oxygen increases tissue oxygen tensions in infected tissue, which allows the aminoglycosides to kill more effectively. Growth and killing studies of Pseudomonas aeruginosa were done aerobically, anaerobically, and under conditions which reproduce the hypoxic levels of infected bone, with reduction of the killing of Pseudomonas aeruginosa by tobramycin under hypoxic conditions. Adjunctive hyperbaric oxygen may also potentiate the bactericidal effect of vancomycin. Under low oxygen tensions, vancomycin, like the aminoglycosides, does not kill micro-organisms as well as under as under normal oxygen levels.

Oxygen is also important in wound healing. When the environment of the fibroblast has an oxygen tension of less than 10 mm Hg, the cell can divide, but it can no longer synthesize collagen. It also cannot migrate to where it is needed for healing. When the oxygen tension is increased, the fibroblast can again carry out these wound healing functions. The collagen produced by these cells forms a protective fibrous matrix, and new capillaries grow into this matrix. Wound healing is a dynamic process, and an adequate oxygen tension is mandatory for this process to proceed to a successful conclusion. HBOT provides oxygen to promote collagen production, angiogenesis, and ultimately wound healing in the ischemic or infected wound. Adequate wound healing is vital in the treatment of osteomyelitis.

Once the bone and soft tissue have been divided, whether by surgery or by infection, the bone and wound must be protected by healing tissues. Bone