HYPERBARIC BIBLIOGRAPHY

(1992-1998)

[Last updated 31 August 1998]

GENERAL INFORMATION AND BASIC SCIENCE

1. Roth RN, Weiss LD. Hyperbaric oxygen and wound healing. Clin. Derm. 1994; 12:141-156.

SUMMARY: [Review of hyperbaric medicine--184 refs.]

Briefly covers historical background for last 300 years, physics and physiology, risks and complications, and contraindications and patient selection. More detailed info provided on acute (clostridial gas gangrene, surgical infections, crush injury, blood loss, burns, brown spider bite) and chronic (diabetic foot, arterial insufficiency ulcers, venous stasis ulcers, radiation injury, osteomyelitis) wound management of specific entities. Hyperbaric oxygen therapy (HBOT) is clinically effective, including its use for the promotion of wound healing. In wound patients it can be cost effective only in extraordinary circumstances, but in the acute wound is a useful adjunct for some life- and limb-threatening situations. In chronic wounds, it can be useful to treat wounds refractory to local medical and surgical care.

2. Brown RB, Sands M. Infectious disease indications for hyperbaric oxygen therapy. Comprehens. Ther. 1995; 21(11):663-7.

SUMMARY: [Brief review of hyperbaric medicine--17 refs.]

Direct costs of HBO are typically around $500 per treatment with chronic indications requiring 20-40 treatments. Article summarizes HBO rationale/delivery and adverse effects and risks, with some elaboration on clostridial myonecrosis, necrotizing soft tissue infection, osteomyelitis, and problem wounds.

3. Burnett JS, Camporesi EM. Hyperbaric oxygen in trauma. In: Grande CM, ed. Textbook of trauma, anesthesia, and critical care. Mosby. 1993.

SUMMARY: [A chapter review on basic physical and physiologic principles of HBO therapy-- 55 refs.]

Treatable entities that are reviewed in this article include: air/gas embolism; DCS; CO poisoning; clostridial myonecrosis; osteomyelitis; crush injury; compartment syndrome; selected non-healing wounds; radiation necrosis; radiation-induced cystitis; blood loss; burns. Anesthesia and its management in hyperbaric medicine, plus a pharmacokinetics discussion if provided.

4. Weiss LD, Van Meter KW. The applications of hyperbaric oxygen therapy in emergency medicine. Am. J. Emer. Med. 1992; 10(2):558-568.

SUMMARY: [A general review of hyperbaric medicine for the emergency physician-- 177 refs.]

Brief overview including physics and physiology, risks and complications, and contraindications. Discussion of emergent indications for hyperbaric oxygen therapy include DCS, gas embolism, CO poisoning, cyanide poisoning, clostridial gas gangrene, surgical infections, crush injuries, compartment syndrome, posttraumatic ischemia, blood loss, and burns. A pithy summary of future applications is presented, including MS and reduction in mycocardial infarct size with hyperbaric oxygen therapy.

5. Kindwall, E. Uses of hyperbaric oxygen therapy in the 1990s. Cleve. Clin. J. Med. 1992; 59(5):517-529.

SUMMARY: [A general review of hyperbaric medicine examining the current indications for HBO therapy-- 70 refs.]

HBO therapy is described for many non-diving and infectious diseases, and other disorders which generally cause hypoxic conditions. Mechanisms of action for HBO are discussed for each of the 12 medical conditions in which there are legitimate criteria indicating the value of hyperbaric oxygen therapy. A brief discussion of the struggle for reimbursement is provided. Some important cost analysis data is briefly covered, for example, patients having burns over 18-39% of their body who receive adjunctive HBO experience an average reduction in their hospitalization from 33 to 20.8 days and decreased cost by $10,850 per case. Physicians are advised to ask seven questions to determine the usefulness of this therapy. Dr. Kindwall concludes that adjunctive HBO is not inexpensive, yet that economic analyses show it to be cost effective. HBO is primarily empirically accepted but is the standard of care for a few specific entities.

ACTINOMYCOSIS

No citations in past 5 years.

CARBON MONOXIDE

1. 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. Ann. Emer. Med. 1995; 25:474-480.

SUMMARY: [(Related editorial also on p. 535. ) 28 Refs.]

Original research. Prospective, randomized study (n=65 patients) with mild to moderate CO poisoning within 6 hours w/o history of loss of consciousness or cardiac instability.

Treatment 1 group (n = 32, mean age = 39): 100% ambient O₂. COHb%: 20.0 d 1.6. Time elapsed until treatment: 1.1 d 0.3 hours. Duration: 4.2 d 0.3 hours.

Treatment 2 group (n = 33, mean age = 35): 30 minutes of 2.8 ATA hyperbaric oxygen followed by 90 minutes of 2.0 ATA hyperbaric oxygen. COHb%: 24.6 d 1.4. Time elapsed until treatment: 1.0 d 0.2 hours. Duration: 2.0 d 0.2 hours.

Delayed neurologic syndrome (DNS) defined as development of new symptoms after oxygen treatment plus deterioration on one or more subtests of a standardized neuropsychologic screening battery given to 60 of the patients.

Results: HBO group of 30 displayed no DNS sequelae. Sequelae developed in 7 of 30 (23%) treated with ambient O₂. DNS occurred 6 d 1 (mean d SE) days after poisoning and persisted 41 d 8 days. One subtest scored worse by Treatment 1 group at 4-week follow-up compared to HBO group and compared to control group matched according to age and education level.

Conclusion: HBO decreased the incidence of DNS after CO poisoning. DNS after CO poisoning cannot be predicted based on patient clinical history or CO level.

2. Hardy KR, Thom SR. Pathophysiology and treatment of carbon monoxide poisoning. Clin. Tox. 1994; 32:613-629

SUMMARY: [A clinical review of epidemiology, pathophysiology, clinical findings and treatment of CO poisoning is provided--115 refs.]

CO poisoning is the leading cause of poisoning in the U.S. A 10-year study through 1988 indicated 56,000 deaths from CO poisoning. Morbidity involving neurological and psychiatric and teratogenic risk is also discussed. Common morbidity includes myocardial and neurologic insult and delayed neurologic sequelae.

The pathophysiology includes hypoxic stress involving diminished red cell O₂ transport and possibly impaired electron transport. CO uptake depends on ventilatory rate, and O₂ saturation tends to remain normal until PaO₂ becomes severely depressed. Carboxyhemoglobin levels confirm the poisoning, but cannot predict severity of poisoning or prognosis, or forecast treatment regimen. No predictive objective measurement for severity of CO poisoning exits. CO can also affect white cells, platelets and the endothelium to result in oxidative injury. A 100-fold plus increase in nitric oxide release from platelets occurs with CO poisoning. Acute mortality from CO appears to be due to ventricular dysrhythmias. Higher risk is associated with a period of unconsciousness or a "soaking" period of exposure longer than one hour, and in those over 60 years of age or having cardiovascular disease.

Treatment rationale is to hasten CO dissociation from hemoglobin even though COHb level has little bearing on a patient’s condition or prognosis. Delay to treatment has adverse effects on recovery. HBO has been shown to prevent CO-mediated oxidative brain injury in animals because it inhibited leukocyte adherence to the microvascular endothelium, a required step in CO pathogenesis. For CO-exposed pregnant females, there is no scientific evidence to depart from standard HBO treatment.

CYANIDE POISONING

No citations in past 5 years on CN poisoning.

DECOMPRESSION SICKNESS AND AIR EMBOLISM

1. Kol S, Ammar R, Weisz G, Melamed Y. Hyperbaric oxygenation for arterial air embolism during cardiopulmonary bypass. Ann. Thorac. Surg. 1993; 55:401-3.

SUMMARY: [Brief Israeli case summary (n = 6) from 1985 to 1993. 16 refs.]

Incidence of arterial gas embolism is estimated at 0.1%, although it may be higher due to instances of non-reporting. Disability is ~ 14% and mortality is ~ 21%. There are ~ 3500 cardiopulmonary bypass surgeries annually in Israel. Causes of AGE include rupture of arterial lines and connectors, oxygenator defects, inadequate arterial reservoir due to insufficient venous return, and sudden acceleration of roller pump.

Rationale for hyperbaric oxygen is compression of bubbles, relieving vascular obstruction and restoring perfusion. HBO also enhances bubble resorption and neural tissue oxygenation and reduces brain edema. The authors claim experience of HBO therapy usefulness even if delay is more than 24 hours after embolization.

2. Pelaia P, Rocco M, Volturo P, Conti G. Arterial air embolism during cardiopulmonary bypass: twelve years experience. J. Hyperb. Med. 1992; 7:115-121.

SUMMARY: [Brief Italian case summary (n = 14) from 1981 to 1992. 19 refs.]

Mortality for AGE is 1%, and 14% develop permanent brain damage. There are no prospective, randomized controlled studies proving the effectiveness of hyperbaric therapy. This study provides the clinical response of 14 patients (11 males and 3 females). Eleven patients were treated within 5 hours onset and three within 24-48 hours. Clinical diagnosis was confirmed in 8 cases by appearance of mydriasis and in 2 cases by transesophogeal Doppler. Patients were invasively monitored and dived to 6 ATA and mechanically ventilated on O₂ , or on nitrox (40/60) at > 2.8 ATA. All received pharmacologic support for brain protection. CT scan was done at 12 and 72 hours post onset.

Results: In all patients, air passage was observed in the extracorporeal circuit. Glasgow coma scores improved. Results of CT scans and neurologic sequelae improved within the first several days, and in four patients neurologic symptomatology disappeared within 3 months. 60% had complete recovery in 48 hours, and 40% in 3 months. All three of the patients in the delayed group remained comatose and died within 20 days. This emphasizes the importance of treatment incipience.

3. Aharon-Peretz J, Adir Y, Gordon CR, Kol S, Gal N, Melamed Y. Spinal cord decompression sickness in sport diving. Arch. Neurol. 1993; 50:753-6.

SUMMARY: [Concise Israeli case summary (n = 68) of 16 years experience in diagnosis/treatment of spinal cord DCS. 33 refs.]

All patients received 100% O₂ and hydration enroute to the hyperbaric medicine therapy, and then 62 received standard US Navy dive table HBO treatment (Table 6, 100% O₂ with air breaks) and 6 received Comex Treatment Table CX-30 (30 meters on 50/50) on helium/oxygen. Presenting symptoms are given.

Full recovery occurred in 79%, and in six of eight patients who continued to have neurological sequelae, spinal symptoms reappeared upon surfacing.

The authors conclude that the US Navy table is not completely safe for treatment of sport divers, and that heliox (50/50) is a promising alternative treatment in severe spinal DCS.

4. Madsen J, Hink J, Hyldegaard O. Diving physiology and pathophysiology. Clin. Physiol. 1994; 14:597-626.

SUMMARY: [Comprehensive Danish review of gas uptake/elimination, bubble formation and DCS and AGE, bubble sequelae, symptomatology, and bubble treatment. > 200 alphabetized refs.]

Gas uptake and elimination issues (involving tissue half-times, modeling, and exposure factors) are introduced. Isobaric inert gas counterdiffusion is briefly covered. Bubble nuclei and de novo bubble formation and their detection with Doppler are discussed. "Silent bubbles" in the venous, low pressure circulation are acknowledged, and are said to be a concomitant observation when symptoms of decompression illness occur. In review, the authors state that 16 of 27 saturated (to 1.48 ata) divers displayed venous bubbles, and in another study venous bubbles were detected (without symptoms) on assent from 1.6 and 1.7 ata saturation dives. For research purposes, N₂O can be used to enlarge extant bubbles because of its solubility and 11X faster entry into the bubbles than N₂ exits.

Sequelae to bubble formation involving platelets, complement, leucocytes, fluid shifts/diuresis/natriuresis, coagulation and other circulatory issues are broached. Bubble growth (in adipose tissue, spinal white mater, and muscle) continues for up to 2 hours on air after decompression, emphasizing the importance of early compression to treat decompression illness.

Dextran demonstrates no difference from Ringer’s lactate in fluid replacement. Antihistamines and smooth muscle activator antagonists may counteract some decompression illness effects. Though no controlled study of corticosteroids has been undertaken, retrospective accounts show benefit, especially in serious neurological DCS and AGE where blood-brain barrier damage and edema are a potential. Heparin, though previously suggested, is no longer advised for the treatment of decompression illness.

Dysbaric osteonecrosis (briefly reviewed here), usually seen years after decompression illness, is an aseptic, probably ischemic disease seen in only 1-2% of navy divers and in 50-65% of Far Eastern commercial divers. Risk increases in saturation and experimental dives, and when there is a history of decompression illness. Pathogenesis is reviewed. Inert gas narcosis, HPNS and liquid breathing are also reviewed.

GAS GANGRENE AND MELENY ULCER (NECROTIZING INFECTION)

1. Hirn M, Niinikoski J, Lehtonen, O.-P. Effect of hyperbaric oxygen and surgery on experimental gas gangrene. Eur. Surg. Res. 1992; 24:356-362.

SUMMARY: [Original work assessing morbidity and mortality in rats comparing no treatment, surgical debridement alone, and combined debridement and HBO following intramuscular injection with Clostridium p. Mortality was 100% in untreated controls, 37% in surgically treated animals, and 12.5% in the HBO experimental group. 16 refs.]

Clostridium perfringens (0.1 ml at a concentration of 10⁸ CFU/ml) in barium sulfate (to localize the nidus) and epinephrine (to cause vasoconstriction and local hypoxia) was used to intramuscularly inoculate Sprague-Dawley female rats. Preliminary experiments showed that ip injection of penicillin (60,000 IU at 45 min. post), prevented fulminate infection and 100% survival, whereas HBO alone without other therapy was not effective, exhibiting 100% mortality.

Control group: (n = 16) received no treatment plus a sham dive (breathing air at ambient pressure)

Treatment group 1: (n = 40) underwent surgery encompassing debridement at 45 min. post-inoculation, followed by thorough irrigation with tap water. (Surgery at greater than 45 min. in this model was not effective, based on preliminary studies.)

Treatment group 2: (n = 40) underwent surgery (as in treatment group 1) plus immediate hyperbaric oxygen therapy (2 ata for 90 min., 5 treatments at 6 hour intervals).

RESULTS: Follow-up assessment lasted 2 weeks. 100% mortality in control group. Treatment group 1 displayed 37% mortality, 50% morbidity and only 12.5% completely healed (healed wound and normal movement). Treatment group 2 showed 12.5% mortality, 12.5% morbidity and 82.5% completely healed. Death usually occurred within 3 days in all groups.

The greatest benefit of HBO is achieved when regional blood flow is intact but local injury and infection have diminished nutrition and oxygen supply to the locally infected tissue.

2. Maisel RH, Karlen, R. Cervical necrotizing fasciitis. Laryngoscope 1994; 104:795-8.

SUMMARY: [Summary of 9 cases from 1983 to 1992. 22 refs.]

The odontogenic and pharyngeal cases grew oral flora, and six cases grew streptococcal species. Anaerobes were in two cases. Extensive surgical exposure of deep cervical fascia occurred. Daily dressing changes and irrigation were aggressive until granulation occurred. Four of 9 patients received HBO (1.5 ata, 1-5 dives at 24 hour intervals). According to one classification method (Klabacha classes I - I V ), these patients fell into the latter two classes involving deep fascia and musculature.

OUTCOMES: All patients survived and displayed scarring, but functional deficits were minimal. The authors selectively use HBO, particularly in deteriorating cases. They cite a retrospective study involving abdominal necrotizing fasciitis that showed 66% mortality in the HBO treatment group, implying this to be more indicative of hyperbaric oxygen therapy results in this type of treatment.

3. Iorianni P, Oliver G. Synergistic soft tissue infections of the perineum. Dis. Colon Rectum 1992; 35:640-4.

SUMMARY: [Less than adequate summary of 7 cases with soft tissue infections of the perineum and urogenital areas that presented between 1987 and 1988. Four of the seven underwent hyperbaric oxygen therapy, 2 or 3 treatments daily, depth/duration??. No conclusive estimation of HBO value was reported, except to say it was of questionable value. 20 refs.]

ACUTE ISCHEMIA AND CRUSH INJURY

1. Zamboni WA, Roth AC, Russell RC, Graham B, Suchy H, Kucan JO. Morphologic analysis of the microcirculation during reperfusion of ischemic skeletal muscle and the effect of hyperbaric oxygen. Plast. Reconstr. Surg. 1993; 91: 1110-1123.

SUMMARY: [Original research into reperfusion and HBO effects in a skeletal muscle ischemia preparation. HBO treatment did not exacerbate reperfusion injury, but rather reduced venular leukocyte adherence and inhibited progressive arteriolar vasoconstriction that developed after the initial vasodilation. 55 refs.]

PREPARATION: Isolated gracilis muscles of 27 rats were transilluminated for videotaping to observe hemodynamics in 101 arterioles and 63 venules. During 3 hours of reperfusion, changes in arteriolar and venular diameter and a determination of leukocyte adherence in 100 m m venular segments were documented.

RESULTS:

Group_________ {results interpolated from figures, not from the abstract}

Treatment group 1: sham, no ischemia {no changes in leukocyte endothelial adherence or arteriolar diameter compared with baseline}

Treatment group 2: 4 hours of global ischemia only’ {elevated leukocyte adherence (~ 15) within 5 min. of reperfusion, and at 3 hours severe vasoconstriction (~ -25%) in arterioles adjacent to venules, but not in those distant from the ischemic venules}

Treatment group 3: no ischemia plus HBO (1 dive at 2.5 ATA for 1 hour) {no changes in leukocyte endothelial adherence or arteriolar diameter compared with baseline}

Treatment group 4: 4 hours of ischemia plus HBO during ischemia {reduced leukocyte adherence (~ + 1% within 5 min. of reperfusion that lasted for three hours), and reduced arteriolar vasoconstriction (~ < 20%)}

Treatment group 5: 4 hours of ischemia plus HBO immediately on reperfusion {reduced leukocyte adherence (<+ 1% at 1 hour following reperfusion), and reduced arteriolar vasoconstriction (~ < 5%)}

Treatment group 6: 4 hours of ishemia plus HBO 1 hour after reperfusion {reduced leukocyte adherence (~ - 5% at 2 hours following reperfusion), and reduced arteriolar vasoconstriction (~ < 10%)}

CONCLUSION: Leukocyte adherence and vasoconstriction (of arterioles adjacent to ischemic venules) are major events in reperfusion injury in muscle, and HBO appears to provide protection by minimizing these effects. Extensive discussion of ischemia injury and a proposed explanation for HBO is provided.

2. Bouachour G, Cronier P, Gouello JP, Toulemonde JL, Talha A, Alquier P. Hyperbaric oxygen therapy in the management of crush injuries: a randomized double-blind placebo-controlled clinical trial. J. Trauma Inj. 1996; 41:333-339.

SUMMARY: [Original research into HBO effects in crush injury (n = 36; 18 in HBO group {100% O₂ at 2.5 ata for 90 min., twice daily for six days}; 18 in placebo group {21% O₂ at 1.1 ata for 90 min., twice daily for six days}). Within 24 hours post-surgery, patients received standard therapies (anticoagulant, antibiotics, wound dressings, and transcutaneous oxygen pressure (P_tCO₂ ) measurements before and during treatment. In the HBO group, 17 completely healed. In the placebo group, 10 completely healed. There were no significant differences in the two groups regarding length of hospital stay and number of wound dressings. BPI (bilateral perfusion index = ratio of transcutaneous oxygen pressure of injured limb to uninjured limb) showed a progressive climb over the first 12 treatments (and achieved normal values by treatment end) in the placebo group whose limbs healed, but did not changed in those patients whose wound did not heal. BPI in the HBO group was constantly greater than 0.9 during hyperbaric oxygen therapy.]

P_tCO₂ before HBO therapy was ~20 mmHg but after 12 sessions was ~ 90 mmHg. A significant improvement in BPI was documented in the HBO group between treatments 1 and 4. Similar improvement in BPI in the placebo group whose wounds were healing was not observed until the 12th treatment. Study end points were: time to wound healing without tissue necrosis requiring surgical excision; new major surgical procedures in relation to progressive and massive revitalization after entry in the trial; time of healing; and length of hospitalization. Repetitive surgical procedures were statistically higher in the placebo group. No significant differences were seen in the time of healing and number of wound dressings, and length of hospitalization was similar.

OSTEOMYELITIS AND OSTEORADIONECROSIS

1. Morrissey I, Smith JT. The importance of oxygen in the killing of bacteria by ofloxacin and ciprofloxacin. Microbios 1994; 79:43-53.

SUMMARY: [Original in vitro study into the dissolved oxygen conditions and redox potentials associated with the bactericidal effect of 4-quinolones (ofloxacin and ciprofloxacin) on E. coli and S. aureus., suggesting that extremely low oxygen levels antagonize 4-quinolone kill. A precise level of oxygen could not be deduced. 20 refs.]

Ofloxacin at its optimum bactericidal concentration (OBC) of 0.9 mg/l was very bactericidal (~ 0.01% survival) at an inoculum size of 107 cfu/ml, but at 1010 cfu/ml was only bacteriostatic (~ 90% survival). Similar results were seen with ciprofloxacin. The overall trend for bacteria treated with quinolones was that the redox potential decreased as the initial inoculum size increased. As long as the pH and temperature of cultures did not vary, cultures with less oxygen showed lower redox potentials than fully aerobic cultures, thus demonstrating that cultures of a high initial inoculum size are much more anaerobic than cultures of a low initial inoculum size even when 4-quinolones were present. At 1010 cfu/ml, the oxygen levels were consumed almost immediately, after 45 min. at 108 cfu/ml, and after 120 min. at 107 cfu/ml. To be effective, the 4-quinolones require high O2 saturation to preclude any antagonism of the bactericidal effect of the drug caused by oxygen consumption by high inoculum sizes.

2. Granstrom G, Fagerberg-Mohlin B, Fornander J, Lindstrom, J, Mercke C. Aspects on the management of patients with osteoradionecrosis after therapy of head and neck cancer. XVIIIth Annual Meeting of EUBS 1992. Joint Meeting on Diving and Hyperbaric Medicine-- 3rd Swiss Symposium, pp. 163-169. [citation incomplete]

SUMMARY: [Original study on osteoradionecrosis (ORN) comparing one retrospective cohort (n = 23 from 1983 to 1988) and one prospective cohort (n = 23 from 1988 to 1992; total of 29 males and 17 females for the two cohorts), the latter cohort receiving adjunctive HBO therapy. Mortality was 27% and 25%, respectively, mean necrosis time was 28 and 15 months, respectively, mean ward time was 10 and 3 months, respectively, and mean antibiotic time was 12 and 3 months, respectively, in the two cohorts. 59 refs]

ORN developed on average at 12 months post-irradiation therapy. No common pathogen was found as etiological for radiation damage. In the prospective group, one patient was classified (according to Marx) as stage 1, and healed. Three were classified as stage 2; two healed, one still had denuded bone. Eleven were classified as stage 3, and all healed. One had the mandible resected but not reconstructed. Two still have progressive ORN. Four died from metastatic malignancy or MI or bronchopneumonia.

After HBO treatment, saliva flow increased and persisted for at least 6 months. Bone reformation could be detected by X-ray films and tomography, and calcium incorporation was detected by microradiography and X-ray diffraction techniques. Blood flow averaged ~ 2 and ~ 6 ml/min · 100 g, respectively, in the non-HBO and HBO groups.

3. Kindwall, E. Hyperbaric oxygen’s effect on radiation necrosis. Clin. Plast. Surg. 1993; 20:473-483.

SUMMARY: [Clinical review of HBO effects in this disease entity. Includes pathophysiology of radiation, effects of hyperbaric oxygen therapy, chamber types, complications of hyperbaric oxygen therapy, current protocols for soft tissue, review of Marx’s three stages, two case reviews, and pictures of a successful treatment of an irradiated buttock wound and mandibular reconstruction following radiation treatment. 24 refs.]

A 20/10 protocol (20 HBO treatments before surgery/10 HBO treatments after surgery) is described. The pre-treatment is used to create well-vascularized tissue that will accept bone grafts. HBO has been shown to have little effect in irradiated neural and eye tissue. Studies are cited indicating that HBO does not stimulate tumor growth, and may have a suppressive effect.

4. Mounsey RA, Brown DH, O’Dwyer TP, Gullane PJ, Koch GH. Role of hyperbaric oxygen therapy in the management of mandibular osteoradionecrosis. Laryngoscope 1993; 103:605-8.

SUMMARY: [Retrospective study of 41 ORN patients treated with HBO from 1980 to 1985. Six (15%) showed complete resolution, and 68% (28) had significant improvement based on at least a 50% reduction in exposed bone, closing of fistulous tract, or complete relief of symptoms; seven (17%) radiologically showed dead bone and demonstrated no HBO benefit. 16 refs.]

General observations: Development of ORN was 6 months to 6 years following radiation therapy. The value of dental extractions remains controversial, an observation made based on the fact that all of the patients had extraction of diseased teeth prior to radiotherapy. HBO was a benefit in the management of ORN. Surgery may be necessary to remove dead bone. All patients with ORN should receive dental evaluation, local wound care, and a strict oral hygiene regimen.

5. Larsen PE, Stronczek MJ, Beck FM, Rohrer M. Osteointegration of implants in radiated bone with and without adjunctive hyperbaric oxygen. J. Oral Maxillofac. Surg. 1993; 51:280-287.

SUMMARY: [Original research in rabbits (n = 20) using contralateral tibias as a control. Adjunctive HBO therapy significantly increased histologic integration of implants and was associated with better soft tissue healing. 20 refs.]

PREPARATION: 20 adult rabbits received unilateral tumorocidal dose of cesium 137 radiation (4500 rad total dose, 10 fractions over 3 weeks) to the proximal tibia, with the contralateral tibia serving as a control. Divided into two groups of 10 each, 5 animals in each group received HBO therapy (2.4 ata for 90 min., once daily, 7 per week for 20 days, with 10 treatments during the first 10 days after implant, 30 total treatments) beginning at 13 weeks post-radiation. Sixteen weeks after the final radiation treatment, cylindrical endosseous implants (titanium plasma-sprayed: n = 5; hydroxyapatite-coated: n = 15) were placed. 10 rabbits (5 HBO, 5 non-HBO) were sacrificed at 12 weeks, and the remaining 10 at 16 weeks.

RESULTS: All implants met the currently used radiographic definition of successful integration, and showed no mobility when subjected to external force at time of sacrifice. In those implants in radiated animals that also received HBO, the histologic picture more closely resembled nonradiated control implants. There was no distinction of integration between implant types (titanium vs. hydroxyapatite) based on statistical comparison.

Allowing more time for integration in the non-HBO group significantly improved the performance of radiated implants. For example, at 12 weeks mean percent integration between radiated and control implants differed by 36.2%, but differed by only 13.9% at 16 weeks. In the HBO group, the 12 and 16 week mean percent integration values differed by 9.5% and 6.38%, respectively, thus showing little improvement by allowing more time for integration in the HBO group.

Obviously, the comparison of HBO and non-HBO groups for the difference in mean percent integration between radiated and control tibia implants at 12 weeks (9.5% vs. 36.2%) demonstrates a significant improvement that is provided by hyperbaric oxygen therapy.

6. Weiss JP, Mattei DM, Neville EC, Hanno PM. Primary treatment of radiation-induced hemorrhagic cystitis with hyperbaric oxygen: 10-year experience. J. Urol. 1994; 151:1514-17.

SUMMARY: [Brief report of 10-year experience with 13 patients with hemorrhagic cystitis treated with HBO therapy and resulting in reversal of tissue injury produced by radiation damage to the bladder. 17 refs.]

Thirteen patients received hyperbaric oxygen therapy (2-hour daily treatments at 2 ata, 60 treatments total, in a monoplace chamber on 100% O₂) after having underwent pelvic radiation for uterine, prostatic, or transitional cell carcinoma and having been admitted to the hospital for intractable hematuria. Bladder complication typically occurs at a 20% rate. In 12 of 13 patients in this study, hematuria resolved to the extent that hospitalization or transfusion were no longer needed. Gross hematuria ceased on average after 33 treatments. One patient required cystectomy and urinary diversion. As described by the authors, these patients represented the severest portion of the bell curve for this illness. HBO is concluded to be an intrinsically reparative treatment.

7. Feldmeier JJ, Heimbach RD, Davolt DA, Brakora MJ. Hyperbaric oxygen as an adjunctive treatment for severe laryngeal necrosis: a report of nine consecutive cases. Undersea Hyperbar. Med. 1993; 20:329-335.

SUMMARY: [Retrospective report of 9 patients from 1980 to 1985 with laryngeal necrosis who underwent hyperbaric oxygen therapy. 28 refs.]

The pathophysiology and a grading system for laryngeal radiation necrosis (rare complication ~ 1%, occurring usually 6-18 months after radiotherapy) is described. HBO (2.4 ata, 3-30 min. O₂ periods separated by 10 min. air breaks once daily, 6/week) treatments were given. Two patients died of complications of secondary malignancies and two died of non-related causes. Two with fistulae healed without surgery, and two underwent surgery for closure. After treatment, seven of nine had good voice quality, and two experienced hoarseness. Several patients experienced temporary change in visual acuity with a tendency toward myopia.

8. Kindwall EP. Hyperbaric oxygen treatment of radiation cystitis. Clin. Plast. Surg. 1993; 20:589-92.

SUMMARY: [Brief literature review and discussion of reported radiation cystitis cases treated with HBO. 4 refs.]

There are few cases reported in the literature, although an informal poll indicates 53 individuals have been treated. HBO appears to be the only form of treatment that reverses the basic vascular pathophysiology induced by radiation. In all of the published cases, major improvement or complete remission resulted.

9. Norkool DM, Hampson HB, Gibbons RP, Weissman RM. Hyperbaric oxygen therapy for radiation-induced hemorrhagic cystitis. J. Urol. 1993; 150:332-4.

SUMMARY: [Report of 14 patients from 1988 to 1991 with radiation-induced hemorrhagic cystitis (reported at a 5.7% to 11.5% rate in large studies) who underwent hyperbaric oxygen therapy (2.4 ata for 90 min., 5-6 days/week averaging 28 treatments for the group). During follow-up from 10-42 months, 8 (57%) had complete resolution of symptoms and 2 (14%) marked improvement. Four (29%) experienced a poor outcome and 3 had recurrent malignancy. One patient was withdrawn from treatment due to illness. Average cost per patient was $10K-$15K. 12 refs.]

10. Lee HC, Liu CS, Chiao C, Lin SN. Hyperbaric oxygen therapy in hemorrhagic radiation cystitis: a report of 20 cases. Undersea Hyperb. Med. 1994; 21:321-7.

SUMMARY: [Report from the Republic of China of 20 females from 1989 to 1992 with radiation-induced hemorrhagic cystitis who underwent hyperbaric oxygen therapy (profile diagrammed: 2.5 ata for 100 min. daily, 6 days/week, averaging 44 treatments for the group). In 16 (80%) patients, macroscopic hematuria was completely halted, and was markedly decreased in 2 (10%). One patient without hematuria but who was experiencing urinary frequency and urgency received 30 treatments with significant improvement. One failed to respond and underwent conduit diversion. HBO was concluded to be safe and effective. 20 refs.]

11. Williams JA, Clarke D, Dennis WA, Dennis EJ, Smith ST. The treatment of pelvic soft tissue radiation necrosis with hyperbaric oxygen. Am. J. Obstet. Gynecol. 1992; 167:412-6.

SUMMARY: [A prospective study of 18 females (previously treated for gynecologic malignancy and who subsequently failed to heal after 3 months) presented with radiation necrosis of the vagina or rectovaginal fistula. Treatment with HBO was provided (2.0 ata in a monoplace chamber for 90-120 min., 1-2 treatments daily, 44 average treatments for the group) were given. Four patients failed to complete treatment, 3 for recurrent disease, and one for anxiety associated with chamber confinement. Only one treatment failure occurred. 13 + 2 refs.]

12. Myers R, Marx R. Use of hyperbaric oxygen in postradiation head and neck surgery. NCI Monogr 1990; 9:151-7.

SUMMARY: [Review of therapeutic use of hyperbaric oxygen in adjunct support of appropriate surgery. Data and comments support use of HBO to treat patients with irradiation complications of head and neck surgery, resulting in improved salvage rates for osteoradionecrosis and its complications (orocutaneous fistula, pathological fractures, bone loss)—33 refs.]

HBO stimulates angiogenesis, increased neovascularization, and optimized cellular O2 for osteoblast and fibroblast proliferation and collagen formation. Acellular, hypoxic matrices in the postirradiated field become hypercellular and normoxic, enhancing healing and recovery. HBO may be used prophylactically in patients with periodontal disease or teeth requiring extraction in a previously irradiated area. HBO helps support flaps and grafts placed into previously irradiated tissue. There is also considerable economic cost saving, improved prognosis, relief of pain, and return of function—all to the patient’s benefit. Physics, gas laws, physiology and therapeutics of HBO are reviewed. Incidence of osteoradionecrosis is examined, and a cost analysis is provided.

SKIN GRAFTS

1. Zamboni WA, Roth AC, Russell RC, Smoot EC. The effect of hyperbaric oxygen on reperfusion of ischemic axial skin flaps: a laser Doppler analysis. Ann. Plast. Surg. 1992; 28:339-41.

SUMMARY: [Original research involving global ischemia (by pedicle clamp occlusion) of epigastric skin flaps in Wistar rats. Control (n = 12) received no HBO. Experimental group 1 (n = 11) received HBO treatment (100% O₂, 2.5 ata for three 1.75-hour treatments with 30 min. air breaks) during ischemia, and experimental group 2 (n = 9) received HBO (2.5 ata for two 1.75-hour treatments with 30 min. air breaks) immediately after ischemia. Laser Doppler (LD) flows were recorded in two distal flap locations at 0.5, 2, 4 and 18 hours after reperfusion in controls and group 1, and at 18 hours after reperfusion in group 2. HBO was concluded to improve distal microvascular perfusion either during or after prolonged global ischemia. 8 refs.]

Total flap ischemia was produced for 8 hours. LD recordings were made during ischemia, also, to document the ischemia produced by the occlusion.

HBO appears to protect the microcirculation from reperfusion injury.

2. Pellitteri PK, Kennedy TL, Youn BA. The influence of intensive hyperbaric oxygen therapy on skin flap survival in a swine model. Arch. Otolaryngol Head Neck Surg. 1992; 118:1050-1054.

SUMMARY: [Original research involving 72 total cutaneous flaps in pigs (n = 12, 6 flaps per pig). Controls (n = 6) received no HBO, and the experimental group (n = 6) received HBO {2.0 ata, 90 min., six treatments on day 1 (surface interval 2 hrs 48 min), five on day 2 (surface interval 3 hrs 9 min), four on day 3 (4 hrs 21 min), three on day 4 (surface interval 6 hrs 21 min), two on day 5 (surface interval 10 hrs 18 min), and one on day 6 (surface interval 12 hrs)}. 24 refs.]

The extent of flap necrosis measuring surface area was determined at necropsy one day following HBO therapy via a digitizer tablet. The area of necrosis (square centimeters) was compared between the two groups.

The authors cite articles which reinforce their viewpoint that the swine skin model is the most clinically applicable animal model for flap research approximating most closely that of the human. They also conclude that, based on a review of the literature, a number of conclusions may be drawn:

• HBO treatment should begin preferably within the first hour following surgery

• pressures > 2 ata appear to offer no benefit

• treatments administered once or twice daily do not improve flap viability

• an optimum period of HBO treatment has not been established.

The authors discuss their philosophy of an aggressive, but tapering schedule of treatment, and state that the last two days of treatment did not produce a discernible change in tissue demarcation (area of necrosis).

3. Stewart RJ, Moore T, Bennett B, Easton M, Newton GW, Yamaguchi KT. Effect of free-radical scavengers and hyperbaric oxygen on random-pattern skin flaps. Arch. Surg. 1994; 129:982-988.

SUMMARY: [Original research in Sprague-Dawley rats involving 10 treatment groups with varying combinations of free radical scavengers (a -tocopherol acetate, superoxide dismutase, catalase) and HBO therapy (2.5 ata, 90 min. daily, within 2 hrs of surgery) or an allopurinol inhibitor with and without HBO. Flap viability was determined by direct observation and fluorescein dye distance (30 min after injection) from the base of the flap on day 7 after surgery. Lipid peroxidation by malondialdehyde (MDA) analysis was also performed. (Because of the nature of the study, an extensive explanation of methods is precluded in this summary.) The combination of treatments significantly increased flap survival except in the group treated with allopurinol and HBO. 40 refs.]

The groups treated with SOD and CAT showed significantly lower levels of MDA (high MDA translates into higher necrosis) compared with the untreated groups, thereby indicating decreased lipid peroxidation. As a side note, the group treated with a -tocopherol demonstrated an average 13% increase in weight compared to weight loss of 2.3% in all other groups.

REGIONAL ENTITIES (DIABETIC, BROWN RECLUSE, VASCULAR WOUNDS) AND BURNS

[Note: some states may have medical society contacts for BRS bites and consultation for HBO treatment, e.g., Arkansas: 1-800-RECLUSE (verified 12-2-96).]

1. Broughton G. Management of the brown recluse spider bite to the glans penis. Mil. Med. 1996; 10:627-9.

SUMMARY: [Case review of brown recluse spider (BRS) bite to the glans penis successfully treated with HBO therapy. 13 refs.]

BRS bites may go unnoticed for days, increasing the chances for tissue necrosis (from sphingomyelinase D, a lipase, which causes dermal necrosis) when not treated quickly. The eschar that develops over the area of necrosis sloughs off leaving an open ulcer, with bacterial infection impeding and delaying healing. Systemic symptoms (fever, chills, malaise, nausea, vomiting, myalgia, urticaria, morbilliform rash, jaundice, hemolytic anemia, renal failure, shock and disseminated intravascular coagulation) may present in 25% of cases. This patient presented with severe buttock pain radiating down both legs and penile pain, neither of which was relieved (treatment included Foley catheter, methylprednisolone sodium succinate IV, diphenhydramine, calcium gluconate, diazepam, magnesium sulfate, lidocaine block of the penis, dapsone PO daily) until he received a spinal caudal block. Within 24 hours the patient received HBO treatment (2 ata for 1 hour, twice daily, 12 total; plus a -tocopherol). Though tissue debridement at other body sites is normal, such treatment may have induced sexual disability. Hyperbaric oxygen therapy was successful with no erectile dysfunction.

2. Maynor ML, Abt JL, Osborne PD. Brown recluse spider bites: beneficial effects of hyperbaric oxygen. J. Hyperb. Med. 1992; 7:89-102.

SUMMARY: [South Carolina facility prospective report on 14 adult patients treated on HBO (2-2.5 ata, 90 min., 1-2X daily in monoplace chamber for 4-7 days) after 3 day follow-up/screen to identify true necrotic envenomation lesions from other differentiating causes. All bites met Auer and Hershey classification III or IV with at least 2-3 cm diameter lesion. All healed without scarring or skin graft, suggesting beneficial effects from hyperbaric oxygen therapy. Two representative cases are presented, and previous studies are reviewed. BRS sequelae and time line are discussed, plus pathophysiology and differential diagnosis. 64 refs.]

3. Maynor ML, Moon RE, Klitzman B, Fracica PJ, Canatia A. HBO and the effect of brown recluse spider venom in rabbits. [Abstract] J. Hyperb. Med. 1993; 20 Supp:45.

SUMMARY: [Original research in rabbits (n = 37) receiving 58 intradermal injections of 73 microliters of venom extract in saline divided into six groups, four of which received HBO. Wound diameter and wound blood flow at day 0, 3 and 7 are presented. HBO significantly decreased wound diameter, but had no noticeable effect on blood flow. Histology indicated more healing in HBO groups compared to controls, and in this study one treatment was as effective as multiple treatments.]

4. Oriani G, Michael M, Meazza D, Sacchi C, Ronzio A, Montino O, Sala G, Campagnoli P. Diabetic foot and hyperbaric oxygen therapy; a ten-year experience. J. Hyperb. Med. 1992; 7:213-221.

SUMMARY: [Report of 172 diabetic patients (108 males, 64 females; 41 patients were eventually excluded based on given criteria) from 1982 to 1992 with extensive ulcerative-necrotic lesions of the lower extremities who underwent strict metabolic control and hyperbaric oxygen therapy (2.5-2.8 ata for 90 min., 5 days/week averaging 40 treatments). A positive outcome was attained for 130 lesions (86%), with 21 (14%) assessed as negative outcomes. The authors no longer regard hyperbaric oxygen therapy as essentially a last attempt therapy. 42 refs.]

5. Wheen L. The effectiveness and cost of oxygen therapy for diabetic foot wounds. SPUMS J. 1994; 24:182-9.

SUMMARY: [Overview article of hyperbaric oxygen therapy indications in diabetes plus cost summaries. Prevalence of diabetic foot ulcers is ~ 10%, with about 1/3 requiring amputation. These amputations account for an average ~ 44% of all amputations, and is usually below the knee. Amputation and vascular reconstruction cost estimates are given. The significance of hypoxia in a diabetic foot wound and the role of oxygen therapy are reviewed. Costs of HBO therapy in the U.S. (mean ~ US$13.5K) and New Zealand (mean ~ NZ$10.5) are presented, and compared to costs of amputation, demonstrating that with added costs of bed stays, amputation and rehabilitation, the HBO group per patient cost was lower. 60 refs.]

6. Wirjosemito, SA. Results of combined therapy including HBO in salvaging diabetic limbs. [Abstract] Aviat. Space Envir. Med. 1992; 440.

SUMMARY: [Retrospective review of 45 diabetic patients treated with HBO (2.4 ata, 140 min., 1-2/day, 35-40 treatments total). 83% were healed.]

7. Hammarlund C, Sundberg T. Hyperbaric oxygen reduced size of chronic leg ulcers: a randomized double-blind study. Plast. Reconstr. Surg. 1993; 93:829-33.

SUMMARY: [Original clinical research looking at patients with non-diabetic, chronic leg ulcers (n = 16) without large vessel disease who were matched by age and wound size and were designated to receive either air or oxygen at 2.5 ata, 90 min., 5 days/week, 30 total treatments. Mean wound area at week 2, 4 and 6 were compared. HBO therapy was concluded to be a valuable adjunct to conventional therapy when nondiabetic wounds do not heal. 12 refs.]

AIR GROUP

WEEK 2-- 2.8 Decrease in Wound Area

WEEK 4-- 3.7% Decrease in Wound Area

WEEK 6-- 2.7% Decrease in Wound Area

O2 GROUP

WEEK 2-- 6% Decrease in Wound Area

WEEK 4-- 22% Decrease in Wound Area

WEEK 6-- 35.7% Decrease in Wound Area

8. Hunt TK. Hyperbaric oxygen reduced size of chronic leg ulcers: a randomized double-blind study. Plast. Reconstr. Surg. 1993; 93:834.

SUMMARY: [Discussion on previous paper. 1 ref.]

9. Giuffrida GF, Giordanengo F, Miani S, Boneschi M, Michael M, Oriani G. Hyperbaric oxygen therapy in the management of trophic ischemic lesions of the lower limbs. 1993. Proceedings of XIXth Annual Meeting of EUBS, Trondheim, Norway. pp. 203-6. (citation incomplete)

SUMMARY: [In a short paper, the authors discuss their experience with 503 patients having ischemic trophic lesions of the lower limb who received HBO therapy. Critical leg ischemia (CLI) is reviewed for classification, and HBO therapy is briefed. Hyperbaric oxygen therapy as a primary or adjunct treatment is concluded to be very efficacious in these lesions. 12 refs.]

10. Cianci P, Sato R. Adjunctive hyperbaric oxygen therapy in the treatment of thermal burns: a review. Burns 1994; 20:5-14.

SUMMARY: [The authors review hyperbaric oxygen therapy in mechanisms and healing effects regarding its beneficial aspects for burns, and provide a rationale for its proactive use to treat burn wounds. Experimental and clinical data are reviewed to show reduced edema, less inflammatory response, reduced hemoconcentration and extravasation, reduced wound surface area, improved dermal survival, enhanced re-epithelialization, reduced need for grafting, decreased hospital stay, and reduced mortality. HBO-treated patients demonstrated an average savings of US $107K per case. HBO treatment is not recommended for trivial burns or when survival chances are minimal, but rather for burns of 20% TBSA or greater, involving hands, face or perineum, and either for partial or full skin thickness burns. Treatment protocols are discussed. 104 refs.]