Hyperbaric oxygen therapy.
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Biomedical subjects
Publications and source records attributed to G B Hart.
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We report the effects of acute smoking cessation on transcutaneous oxygen (PtcO2) measurements in room air and with hyperbaric oxygen (HBO2) of an extremity at risk for amputation. The reports on cigarette smoking and PtcO2 do not discuss acute smoking cessation. PtcO2 measured 46 h after smoking cessation increased 10% while breathing room air and 34% with HBO2, as compared to measurements made before smoking cessation.
In a previous pilot study, we demonstrated that adjunctive treatment with hyperbaric oxygen (HBO) appears to be feasible and safe in patients with acute myocardial infarction (AMI) and may result in an attenuated rise in creatine phosphokinase (CPK), more rapid resolution of pain and ST changes. This randomized multicenter trial was organized to further assess the safety and feasibility of this treatment in human subjects. Patients with an AMI treated with recombinant tissue plasminogen activator (rTPA) or streptokinase (STK), were randomized to treatment with HBO combined with either rTPA or STK, or rTPA or STK alone. An analysis included 112 patients, 66 of whom had inferior AMIs (p = NS). The remainder of the patients had anterior AMIs. The mean CPK at 12 and 24 h was reduced in the HBO patients by approximately 7.5% (p = NS). Time to pain relief was shorter in the HBO group. There were 2 deaths in the control and 1 in those treated with HBO. The left ventricle ejection fraction (LVEF) on discharge was 51.7% in the HBO group as compared to 48.4% in the controls (p = NS). The LVEF of the controls was 43.4 as compared to 47.6 for those treated, approximately 10% better (no significant difference). Treatment with HBO in combination with thrombolysis appears to be feasible and safe for patients with AMI and may result in an attenuated CPK rise, more rapid resolution of pain and improved ejection fractions. More studies are needed to assess the benefits of this treatment.
Hyperbaric oxygen treatment (HBO) in combination with thrombolysis has been demonstrated to salvage myocardium in acute myocardial infarction in the animal model. Therefore a randomized pilot trial was undertaken to assess the safety and feasibility of this treatment in human beings. Patients with an acute myocardial infarction (AMI) who received recombinant tissue plasminogen activator (rTPA) were randomized to treatment with HBO combined with rTPA or rTPA alone. Sixty-six patients were included for analysis. Forty-three patients had inferior AMIs (difference not significant) and the remainder had anterior AMIs. The mean creatine phosphokinase level at 12 and 24 hours was reduced in the patients given HBO by approximately 35% (p = 0.03). Time to pain relief and ST segment resolution was shorter in the group given HBO. There were two deaths in the control group and none in those treated with HBO. The ejection fraction on discharge was 52.4% in the group given HBO compared with 47.3% in the control group (difference not significant). Adjunctive treatment with HBO appears to be a feasible and safe treatment for AMI and may result in an attenuated rise in creatine phosphokinase levels and more rapid resolution of pain and ST segment changes.
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Hyperbaric oxygen therapy is an important adjunct in the management of respiratory injuries secondary to smoke inhalation, especially when injury is complicated by inhalation of a toxic chemical such as carbon monoxide or cyanide. For carbon monoxide poisoning, such therapy has become a standard of practice. As more information becomes available concerning the ability of hyperbaric oxygen to reduce reperfusion injuries, we anticipate that this therapy will become a standard of practice for managing smoke inhalation injuries and cyanide poisoning as well.
This study examines the effect of delayed exposure to hyperbaric oxygen on muscle necrosis and edema development following compartment syndromes in the canine hindlimb. Compartment syndromes (100 mm Hg for 8 h) were generated in one anterolateral compartment of six anesthetized dogs. After a 2-h delay, three 1-h hyperbaric oxygen treatments (2 atm absolute pure oxygen) were given during the next 12 h. Two days later, technetium-99m stannous pyrophosphate (99mTc Sn-PYP) was injected intravenously; 3 h later, samples were obtained from the pressurized and contralateral control muscles, weighed for edema development, counted for 99mTC Sn-PYP uptake, and evaluated histologically. Hyperbaric oxygen treatments, even when delayed 2 h, reduced muscle necrosis and intramuscular edema to negligible levels (p less than 0.05) compared with untreated animals. In addition, muscle morphology remained essentially normal in all hyperbaric oxygen-treated animals. We conclude that even if hyperbaric oxygen treatments are delayed 2 h, edema and muscle necrosis are reduced significantly in a model compartment syndrome.
Hyperbaric oxygen therapy has a marked beneficial effect in experimental intraabdominal sepsis. Two rat models involving implantation of either rat fecal material or a mixture of pure cultures of Escherichia coli, Streptococcus faecalis, and Bacteroides fragilis were used in this study. A death rate of 100% was obtained in control animals implanted with fecal material; with intermittent hyperbaric oxygen treatment, a death rate of only 8% was observed (P less than .005). With a mixture of pure cultures of clinical pathogens, the death rate in control animals was 79%, and intermittent hyperbaric oxygen treatment reduced the rate to 23% (P less than .005). Data from cultures of blood indicated that the efficacy of hyperbaric oxygen was not related to antibacterial activity.
This study examined the effect of exposures to hyperbaric oxygen on the development of the edema and necrosis of muscle that are associated with compartment syndromes that are complicated by hemorrhagic hypotension. A compartment syndrome (twenty millimeters of mercury for six hours) was induced by infusion of autologous plasma in the anterolateral compartment of the left hind limb of seven anesthetized dogs while the mean arterial blood pressure was maintained at sixty-five millimeters of mercury after 30 per cent loss of blood volume. These dogs were treated with hyperbaric oxygen (two atmospheres of pure oxygen) and were compared with six dogs that had an identical compartment syndrome and hypotensive condition but were not exposed to hyperbaric oxygen. Forty-eight hours later, edema was quantified by measuring the weights of the muscles (the pressurized muscle compared with the contralateral muscle), and necrosis of muscle was evaluated by measuring the uptake of technetium-99m stannous pyrophosphate. The ratio for edema was significantly (p = 0.01) greater in dogs that had not been exposed to hyperbaric oxygen (1.15 +/- 0.01) than in the dogs that had been treated with hyperbaric oxygen (1.01 +/- 0.03), and the ratio for necrosis of muscle was also significantly (p = 0.04) greater in dogs that had not had hyperbaric oxygen (1.96 +/- 0.41) than in those that had been treated with hyperbaric oxygen (1.05 +/- 0.11). Comparisons were also made with the muscles of four normal control dogs and separately with the muscles of six normotensive dogs that had an identical compartment syndrome and normal blood pressure and were not treated with hyperbaric oxygen.(ABSTRACT TRUNCATED AT 250 WORDS)
Five patients with smoke inhalation from house fires presented to the hospital in a comatose state. Carboxyhemoglobin levels were elevated in all five patients, mean=32% +/- 6. Arterial blood gases revealed the following means: pH 7.16 +/- 0.06; PCO2 35 mm HG +/- 10.5; HCO3 12.6 mEq/L +/- 0.07; base excess -16 mEq/L +/- 1.58; PO2 353 mm Hg +/- 149; O2 saturation 66% +/- 5.5. The patients were presumed to have both cyanide and carbon monoxide intoxication and were treated with the cyanide antidote kit and hyperbaric oxygen (HBO). Four of five patients awoke within 15 minutes of reaching maximum pressure and remained neurologically intact thereafter. The fifth patient died one week later. Cyanide blood levels drawn prior to treatment revealed a mean of 1.62 microgram/mL +/- 1.44. The highest cyanide level was 3.9 microgram/mL (the death) and the lowest 0.35 microgram/mL. We conclude that smoke inhalation can result in acute cyanide poisoning and that hyperbaric oxygen is a useful adjunct in the treatment of smoke inhalation.
Hydrogen sulfide inhalation injury can be life threatening. The toxic gas is produced, sometimes unexpectedly, from a wide variety of sources. Because its mechanism of toxicity is similar to that of cyanide, hydrogen sulfide poisoning is commonly treated with the nitrite component of the cyanide antidote kit. In this case report, hyperbaric oxygen was successfully used to treat hydrogen sulfide intoxication. Further evaluation of hyperbaric oxygen therapy as adjunctive treatment of hydrogen sulfide poisoning is recommended.
Spinal Cord Injury patients are liable to develop osteomyelitis mostly by extension from pressure ulcers. In 2055 records reviewed in the Long Beach Spinal Cord Injury Service of the Veterans Administration Medical Center, the incidence was found to be 4.3 per cent. Of these osteomyelitis developed secondary to pressure ulcers in 88 per cent, the rest developed as a result of trauma and/or surgery. Forty-four patients manifesting chronic osteomyelitis were treated in a monoplace hyperbaric oxygen (HBO) chamber, in addition to receiving antibiotic and surgical treatment. HBO was found useful as an adjunct to help to resolve the bone infection and encourage wound healing. Two-thirds of the patients were cured, and the follow-up was from 6 months to 9 years. We believe that HBO is a useful adjunctive therapeutic measure in the management of chronic osteomyelitis in the spinal cord injured and in the prevention of its complications.
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Gas gangrene is not a disease of the past. Despite improved awareness, earlier care of trauma victims, new antibiotics, and advanced monitoring techniques, histotoxic clostridia continue to cause loss of life and limb. A 20-year literature review on gas gangrene (Part I) indicates that a combined therapy approach with early recognition, surgical intervention, appropriate antibiotics, and hyperbaric oxygen (HBO) provides optimal care. Part II, a 15-year clinical experience, appears to be the largest English-language series reported using the combined therapy of antibiotics, surgery, and hyperbaric oxygen. One hundred thirty-nine patients (95 males and 44 females), average age, 38 years, were admitted with clostridial myonecrosis. Sixty-seven were in shock at admission and the 27 deaths occurred in this group. One hundred twelve patients (81%) survived the infection. There was a 5% mortality in post-traumatic extremity clostridial myonecrosis. Age and concurrent disease increased the mortality rate, as did delay from time of diagnosis to aggressive combined treatment.
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Eight human volunteers, individually studied in a hyperbaric chamber, breathed: 1) air at 1 ATA; 2) 80% argon and 20% oxygen and 1 ATA for 30 min; 3) air at 1 ATA for 30 min; 4) 100% 02 at 1 ATA for 30 min; 5) air at 1 ATA for 30 min; 6) 100% O2 at 2 ATA for 60 min; and 7) 80% argon and 20% oxygen at 1 ATA for 30 min. Oxygen, carbon dioxide, nitrogen, and argon tensions were measured in muscle and subcutaneous tissue by mass spectroscopic analyses. Venous blood obtained at regular intervals was analyzed for coagulation and fibrinolytic factors. Inert gas narcosis was not observed. After breathing argon for 30 min, muscle argon tensions were almost three times subcutaneous tensions. Argon wash-in mirrored nitrogen wash-out. Argon wash-in and wash-out had no effect on tissue Po2 or Pco2. Coagulation and fibrinolytic changes usually associated with vascular bubbles were absent.
Of 70 patients with refractory osteomyelitis who received treatment with hyperbaric oxygen, all improved and 63% have remained free of disease. Treatment is supplemental to properly timed surgery and antibiotic therapy.