Undersea & hyperbaric medicine: journal of the Undersea and Hyperbaric Medical Society, Inc

We investigated the effects of an elevated ambient air pressure of 0.6 MPa on verbal memory performance. Twenty-four experienced divers were compressed in a dry hyperbaric chamber to pressures equivalent to 0.5 meters of seawater (msw) (n = 12) and 50 msw (n = 12). Verbal memory was assessed by free recall and recognition of visually presented word lists. The testing procedure specified learning and testing at surface, learning at surface and testing at depth, learning and testing at depth, and learning at depth and testing at surface. Non-specific stress was assessed by measurement of salivary cortisol, heart rate, and subjective stress before, during, and after the dives. The 50-msw dive group showed a significant decrease of free recall performance when the material was learned at depth (P < 0.01). However, only postdive recall of material learned at depth remained significantly impaired (P < 0.05), whereas recognition performance was normal. For both groups no significant effects of depth on the investigated stress indices were obtained. These results are taken as evidence that inert gas narcosis may interfere with encoding and/or retrieval of verbal information, although the possibility that other stressors in the hyperbaric environment contributed to these deficits cannot be eliminated entirely.
The U.S. Navy recommends submarine escape for depths down to 600 fsw, with deeper escapes entailing the risks of decompression sickness, nitrogen (N2) narcosis and CNS oxygen (O2) toxicity. However, the escape equipment, including the submarine escape and immersion equipment and the escape trunk, could probably function even at 1,000 fsw. Here we report a theoretical analysis of the risks of both N2 narcosis and CNS O2 toxicity for different escape profiles from 600 to 1,000 fsw. The effect of N2 narcosis, calculated as a function of N2 pressure in the brain using Gas Man software, was expressed as equivalent narcosis depth (END), corresponding to the depth at which the same pressure of N2 would be produced in the brain after five minutes of scuba diving with air. The risk of O2-induced convulsions was estimated using the model developed by Arieli et al. Different dwell times (DTs) at maximal pressure in the escape trunk (from 0 to 60 s) and lungs-to-brain circulation times (10 to 30 s) were included in our analysis. When DT in the escape trunk is very short (e.g., 10 s), the risk of either incapacitating N2 narcosis and/or O2-induced convulsions occurring in the trunk is low, even during escapes from 1,000 fsw.
Nitrogen (N2) narcosis could interfere with deep submarine escapes, particularly in the escape trunk, where simple but essential tasks are required in order to leave the submarine and start rapid ascent. In a previous study, we had suggested that prolongation of lungs-to-brain circulation time (LBct) may have a protective effect on N2 narcosis, a hypothesis tested in the present study. Computer software was designed to assess the effects of changes in circulation times on N2 uptake and distribution during the extremely rapid pressure changes typical of submarine escapes. Simulations of escapes from 600 to 1,000 fsw (with 200-fsw steps) were performed, with varying dwell times (DT) in the escape trunk (from 10 to 60 seconds, in 10-second steps). Baseline cardiac output (CO) was set at 5 liters/minute, and it was varied through changes in heart rate from 50% to 200% in the escape simulations. LBct was assumed to vary inversely with CO. The risk of N2 narcosis was expressed as equivalent narcosis depth (END) in fsw, corresponding to N2 pressure in the brain after five minutes of air diving at that equivalent depth. The effects of changing CO on the highest END values (corresponding to the peak N2 pressures) reached while in the escape trunk or during entire escapes were tabulated. Depths at which peak N2 occurred were also analyzed. Prolonging LBct appeared to have two advantageous effects: 1. It reduced peak N2 reached both in the escape trunk and during the entire course of the escape 2. It delayed peak N2 to later stages of escapes (i.e., closer to the surface during ascent). These effects were more evident at greater escape depths and with longer DTs. Prolongation of LBct could protect against N2 narcosis and it could plausibly be achieved with the oral administration of a beta-blocker, such as propranolol, prior to deep submarine escape. Animal experiments should be conducted to validate this pharmacological approach.
Four divers were chosen as subjects to conduct the 1,100 kPa He-O2 simulated saturation dive. Brainstem auditory evoked potentials of the divers were monitored during different stages of the exposure. At 1,100 kPa, with both 10 and 50 Hz clicks, interpeak latencies I-V were prolonged by 0.242 and 0.360 ms, respectively, indicating impedance of synaptic transmission. Results showed that interpeak latencies I-V were prolonged by 0.242 and 0.360 ms, respectively, indicating impedance of synaptic transmission. However, the latency of wave I was shortened by 0.11 ms, which was presumed to be due to different mechanical sound transmission velocity at hyperbaric helium environment. Interestingly, the latency of wave I prolonged gradually during hyperbaric exposure to 1,100 kPa. This might be used for the measurement of effects of hydrostatic pressure and He on the central nervous system (CNS). These changes coupled with easy perspiration and fatigue of the divers suggest that the pressure of the present experiment had certain effects of the CNS on the divers, although they were moderate and temporary.
In order to evaluate the effects of ambient pressure on reaction and movement times we investigated 60 professional divers by a computerized test (Reaction Test). The experiments were carried out four times in a hyperbaric chamber: prior to pressure, at 6.0 and 1.9 atm abs and after decompression. Reaction time varied from 202 to 443 milliseconds (275 +/- 42 ms), but the individual levels remained similar. The reaction time increased between precompression and 6.0 atm abs (p < 0.05), decreased between 6.0 and 1.9 atm abs (p < 0.05) and remained at the original level at 1.9 and 1.0 atm abs after decompression. Ten divers had an increase of more than 1SD in the reaction time at 6.0 atm abs. The number of mistakes was small and not influenced by elevation of pressure. Further, the movement time remained unchanged throughout the experiment. We conclude that the response time increases due to ambient pressure and the increase in simple reaction time is detectable in professional divers at 6.0 atm not at 1.9 atm abs. At the same time accuracy stays constant. We speculate that our findings are caused by nitrogen narcosis in some divers.
Tumor cell kinetics were studied in C57 Bl/J mice with a transplantable sarcoma, MCG 101, exposed to hyperbaric oxygen (HBO2), 2.8 atm abs, 2 hours daily for 9 days or until spontaneous death. The isoenzymatic pattern of lactate dehydrogenase (LDH) confirmed that there was a significant shift toward aerobic metabolism in tumor tissue as well as in the liver and skeletal muscle. Recruitment of cells from the G0G1 state into DNA synthesis was associated with an increased mobilization of substrates for polyamine synthesis in terms of an elevated ornithine decarboxylase (ODC) activity. However, cell cycle turnover in terms of bivariate flow cytometric analysis after bromodeoxyuridine (BrdUrd) injection, final tumor weight, and survival time were not changed compared with the controls. Tumor cell metabolism demonstrated evidence of an unchanged net energy utilization, in that activities (V(max) of phosphofructokinase (PFK) and LDH were not significantly changed. When the tumor-bearing animals were exposed to advanced HBO2 pressure (3.7 atm abs) for 3 h as a single dose, the DNA distribution and growth rate were not changed immediately. However, 3.5 h later we observed a DNA pattern similar to that after repeated HBO2 treatments, 2.8 atm abs, concomitant with a preponderance of cells in the late S-phase, which is consistent with a block at the entry of G2M. We conclude that MCG 101 sarcoma recovers from HBO2 exposure by an accumulation of cells in the S-phase without significant changes of net tumor growth. This may have relevance to clinical radiocurability.
Saturation diving involves the exposure of humans to elevated partial pressure of oxygen (PO2) and high ambient pressure. The present study is part of a research program that focuses on how such conditions affect basal cellular functions. C3H/10T1/2 Cl 8 mouse embryo fibroblasts were exposed to 20-80 kPa O2 in a He-O2 mixture at 0.1 and 5.0 MPa ambient pressure for 24-72 h. Elevated PO2 had severe toxic effects on the cells, and there was an additional effect of high pressure on net cell growth. A persistent reduction of cell growth rate after the end of exposure to He-O2 was noted, suggesting genetic effects. We observed no effects of the ambient pressure per se in this respect. High PO2 increased the cellular glutathione level reaching a plateau approximately 100% above control at a PO2 of 60 kPa. No alteration of the glutathione redox status was observed, and high ambient pressure per se had no significant effect on the cellular glutathione content. The increased glutathione content did not completely protect the cells against toxic injury of high oxygen levels.
We examined the effect of a prolonged dive on measures of oxidative stress in human divers. Ten subjects, wearing dry suits, completed mental tasks while lying quietly at 4.6 m fresh water for 3.5 h. Subjects (9 male, 1 female) were active, experienced divers ranging in age from 19 to 54 yr. Subjects breathed an enriched air nitrox mixture yielding a P(O2) of approximately 120 kPa(a) for the duration of the dive. Venous blood was drawn before and after the dive for measurements of hemoglobin (Hb), hematocrit (Hct), plasma osmolarity (O(SM)), red blood cell osmotic fragility (Frag), superoxide dismutase activity (SODa), and thiobarbituric acid reactive substances (TBARS). Plasma volume (PV) shifts were calculated from the changes in Hb and Hct. Significant increases in Hb, Hct, Osm, Frag, and TBARS were found along with significant decreases in PV and SODa (P < or = 0.05). We conclude that hyperbaric exposures encountered by technical divers are sufficient to cause significant oxidative stress.
To detect cumulative effects of and check required recovery times between underwater exposures to 130-140 kPa oxygen, we assessed pulmonary oxygen toxicity after resting dives for four and six hours on two, five, and six or ten days, and three hours twice on each of two days. Despite a slight downward trend in diffusing capacity, four-hour resting dives could be repeated for at least ten days if intervals between them were 20 hours: 17% of divers had mild symptoms; 5%, mild changes in flow-volume parameters. In contrast, six-hour resting dives caused symptoms in 33% of divers. When dives were repeated daily (after 18 hours), but not with one day off (after 42 hours), changes in diffusing capacity accumulated, and hyperoxic myopia occurred after five dives. Divers complained of fatigue more with daily than with alternate day dives. When daily exposure was split into two three-hour dives, the incidences of symptoms and changes in pulmonary function depended on the surface intervals: on the second day, with two and 16 hours between dives, two three-hour dives were similar to a six-hour dive; with four and 14 hours, to a four-hour dive; with six and 12 hours, to a six-hour dive.
Pulmonary effects of prolonged mild intermittent underwater cycle ergometer exercise were assessed after single and repeated four-hour dives to 12 feet. With air, five daily dives (surface interval [SI], 20 hours), and with 100% oxygen, single dives, five daily dives, and afternoon-morning dives (SI, 15 hours) were conducted. Air divers had no symptoms or abnormal pulmonary function values but showed slight decreases within the normal range in forced expired volume in one second (FEV1; -0.45%/day) and forced expired flow between 25% and 75% of volume expired (FEF25-75; -0.8%/day). After one oxygen dive, incidences of mild symptoms or reduced pulmonary function were not different with exercise from those resting, but during five dives, decreases were significant in FEF25-75 (-1.8%/day) and diffusing capacity of the lung for carbon monoxide (D(L)CO; -1.2%/day), estimated to cause abnormal values in 25% of divers in nine to ten days. Following afternoon-morning dive pairs, changes in FEV1 and FEF25-75 were similar to those after nine or four daily dives, respectively. Exercise increases the injurious pulmonary effects of 140 kPa oxygen, and oxygen, those of exercise. A one-day break should follow two 4-hour exercise oxygen dives with surface intervals of 15 to 20 hours.
Elevated inspired oxygen partial pressures (PO2) may cause pulmonary oxygen toxicity (PO2T). However, normal variability and water immersion also cause pulmonary function (PF) changes. In 21 subjects, we measured the variability of flow-volume parameters and diffusing capacity for carbon monoxide (DLCO) for six weeks without diving. In 24 divers, we compared the effects of air (P(I)O2 = 0.3 atm = 30 kPa) and oxygen (P(I)O2 = 1.4 atm = 140 kPa) during paired resting dives of 4, 6, or 8 hours in a freshwater pool 4.6 m deep. Without diving, median coefficients of variation (CV) were: vital capacity, 3.2%; FEV1, 3.5%; peak flow, 7.0%; and DLCO, 5.9%. Measurements within 2.4.CV of baseline were considered unchanged. After 4-, 6-, and 8- hour air dives, PF decreased in one, one, and four subjects, respectively, and three, one, and two, respectively, reported symptoms. After the oxygen dives, PF decreased in two, three, and four subjects, respectively, and two, four, and seven, respectively, reported symptoms. PO2T persisted for several days after 8-hour oxygen dives.
The aim of this work was to identify clinical data indicative of the number of hyperbaric oxygen therapy HBO2 sessions that should be prescribed for adjuvant treatment of tissue injuries of differing severity. A total of 1730 cases of patients treated with HBO2 using an open protocol (without a predetermined number of sessions) was examined in this study. A retrospective study involving charts review was conducted. Severity had been previously determined for the treatment of acute (fasciitis, myositis, gangrene, contaminated/infected perineal or lower extremity traumatic injuries) or chronic (osteomyelitis, pressure sore, diabetic or ischemic ulcer) injuries. Only patients that met or exceeded the supposed effective minimal treatment doses (5 sessions for acute, 10 sessions for chronic injuries) were included in the present study. The data analysis included 1506 cases. These consisted of 1014 patients with acute injuries, who required 11 to 18 sessions (depending on injury severity), and 492 patients with chronic injuries, who required a greater (p < 0.001) number of sessions (approximately 30/patient, independent of injury severity). Global mortality was 79/1506 patients. These results seem to support the initial indication of 15 HBO2 sessions for the treatment acute injuries, and 30 for treatment of chronic injuries. Prospective studies may better determine the number of sessions for the treatment of different types of injuries.
When going to high altitude (higher than 2,400 meters above mean sea level [about 8,200 feet]), human physiology is strongly affected by changes in atmospheric conditions, including decreased ambient pressure and hypobaric hypoxia, which can lead to severe hypoxemia, brain and/or pulmonary edema, negative changes in body and blood composition, as well as disturbances in regional microcirculation. When adding other factors, such as dehydration, physical exercise and exposure to low temperature, it is likely that nitrogen desaturation after diving at such environmental conditions is far from optimal, There are only single reports on diving at high alti-tudes. In 2007 a Polish team of climbers and divers participated in the Tilicho Lake and Peak Expedition to the Himalaya Mountains in Nepal. During this expedition, four divers conducted six dives in the Tilicho Lake at altitude of 4,919 meters above mean sea level equivalent (16,138 feet) to a maximum depth of 15 meters of fresh water (mfw) (equivalent to 28 mfw at sea level by the Cross Correction method) and 30 mfw (equivalent to 57 mfw at sea level "by Cross correction). Decompression debt was calculated using Cross Correction with some additional safety add-ons. Precordial Doppler recordings were taken every 15 minutes until 90 minutes after surfacing. No signs or symptoms of decompression sickness were observed after diving but in one diver, very high bubble grade Doppler signals were recorded. It can be concluded that diving at high altitude should be accompanied by additional safety precautions as well as taking into account personal sensitivity for such conditions.
Many divers report less fatigue following diving breathing oxygen rich N2-O2 mixtures compared with breathing air. In this double blinded, randomized controlled study 11 divers breathed either air or Enriched Air Nitrox 36% (oxygen 36%, nitrogen 64%) during an 18 msw (281 kPa(a)) dry chamber dive for a bottom time of 40 minutes. Two periods of exercise were performed during the dive. Divers were assessed before and after each dive using the Multidimensional Fatigue Inventory-20, a visual analogue scale, Digit Span Tests, Stroop Tests, and Divers Health Survey (DHS). Diving to 18m produced no measurable difference in fatigue, attention levels, ability to concentrate or DHS scores, following dives using either breathing gas.
The objective assessment of the extent of cerebral insult and the effects of therapy in decompression injury patients has proven to be difficult by most imaging modalities. In this pilot study we evaluated the ability of 18-F-2-fluoro-2-deoxyglucose (FDG) positron emission tomography (PET) to identify metabolic brain abnormalities in decompression injury patients. Twenty-two patients who were evaluated at our institution for decompression accidents were evaluated with FDG-PET. Four of the 22 patients had no neurologic symptoms and no neurologic findings on clinical exam at the time of the FDG-PET study. No statistically significant correlations were found between the presence of symptoms and the demonstration of abnormalities on the PET study and no statistically significant correlation was found between the location of the decompression injury and the demonstration of abnormalities on the PET study. We conclude that FDG-PET imaging of the brain cannot reliably identify cerebral abnormalities in patients with decompression injuries and would be of limited benefit for monitoring therapy in patients with decompression illness.
The contents of oxygen free radicals (OFRs) and malondialdehyde (MDA) in S-180 sarcoma tissues were measured in four groups of mice: an untreated normoxic group, a normoxic hyperbaric group, a hyperbaric oxygen group, and an HBO group treated with superoxide dismutase (SOD). Measurements were done by electron resonance and spectrophotometry, and observations were made on the volume, weight, necrosis incidence rate of sarcoma tissues, and mortality in all groups. The OFR and MDA content in sarcoma tissues in the HBO group was significantly higher than those of the control groups (P < 0.001); necrosis incidence of sarcoma tissues and the survival rate of mice were higher; the time required for necrosis was shorter, and the volume and weight of sarcoma tissues were smaller and lighter than those of the control groups (P < 0.01). The results suggest that SOD cannot completely eliminate OFRs produced by hyperbaric exposure, although the role of HBO in producing more OFRs can be counterbalanced by SOD to a certain degree. Apparently HBO can check the growth rate of sarcoma and accelerate the necrosis of S-180 sarcoma cells.
In order to investigate causative factors, root cause analysis (RCA) was applied to 351 Australian compressed-gas diving fatalities from 1972-2005. Each case was described by four sequential events (trigger, disabling agent, disabling injury, cause of death) that were assessed for frequency, trends, and dive and diver characteristics. The average age increased by 16 years, with women three years younger than men annually. For the entire 34-year period, the principal disabling injuries were asphyxia (49%), cerebral arterial gas embolism (CAGE; 25%), and cardiac (19%). There was evidence of a long-term decline in the rate of asphyxia and a long-term increase in CAGE and cardiac disabling injuries. Asphyxia was associated with rough water, buoyancy trouble, equipment trouble, and gas supply trouble. CAGE was associated with gas supply trouble and ascent trouble, while cardiac cases were associated with exertion, cardiovascular disease, and greater age. Exertion was more common in younger cardiac deaths than in older deaths. Asphyxia became less common with increasing age. Equipment-related problems were most common during the late 1980s and less so in 2005. Buoyancy-related deaths usually involved loss of buoyancy on the surface but decreased when buoyancy control devices were used. Countermeasures to reduce fatalities based on these observations will require validation by active surveillance.
This paper reports on the outcomes and efficacy of the deep treatment schedules employed at the University of Hawaii to treat diving accident victims. These tables utilize increased atmospheric pressures, several mixed gas combinations, and a more gradual staged decompression rate than US Navy treatment schedules. The majority of our study population (72.4%) was treated using a single specific treatment schedule. 90% were treated using deep tables either singly or in combination with other tables. 91.6% of cases treated on deep tables achieved complete functional recovery. The percentage of cases obtaining complete functional recovery ranged from 91.3% to 99% based upon condition treated, and from 77.5% to 100% based upon treatment schedule employed. Number of treatments required by type of injury ranged from 1.3 to 2.4 treatments. 74.5 % of cases required two or less treatments to obtain complete functional recovery. Severity of injury and age of the diver were the most sensitive predictors of outcome while delay to treatment did not influence outcomes in this study population.
Histograms showing the numbers of divers in each age range for both IDDM and NIDDM divers. 
Graph of Kaplan-Meier survival estimates for the length of time that IDDM and NIDDM divers participate in the survey and that divers with the BSAC remain members of the club. 
To survey the outcomes and practises of divers with diabetes mellitus. Diabetic persons wishing to learn to scuba-dive or established divers who have diabetes mellitus in the UK are requested to fill in a detailed questionnaire annually. Divers are asked to provide basic epidemiological information and general diving history. Data provided by the diver's diabetic physician provided independent evidence of the diver's medical status. These data are recorded and analysed. Data have been gathered from 323 diabetic divers (269 male, 54 female) and 8,760 dives have been recorded over 11 years. Two fatalities were reported, both in non-insulin dependent divers. One incident of hypoglycaemia underwater in an insulin dependent diabetic diver has been reported. This survey showed that in the group of well-controlled diabetic divers studied, there were no serious problems due to hypoglycaemia when they dived. Long-term complications of diabetes must be excluded before a diabetic diver may be permitted to dive.
Brain auditory evoked potential (BAEP) in mice exposed to hyperbaric H2O2 pressure was monitored to reveal the correlation between altered synaptic transmission and hydrogen narcosis or isobaric HPNS. Inter peak latencies and wave amplitudes were selected as indices of assessment. The animals were exposed either to He-O2 or H2-O2 at 2.1 MPa and 4.1 MPa. Results showed that synaptic transmission was inhibited to various extents. The inhibition was partly due to the narcotic effect of hydrogen, which was added to the effect caused by hydrostatic pressure. On the other hand, asymmetrical reaction of each segment in the neuro-network might be responsible for the occurrence of HPNS.
Neurological complications are common in recreational divers diagnosed with decompression illness (DCI). Prior reports suggest that hemoconcentration, with hematocrit values of 48 or greater, increase the risk for more severe and persistent neurological deficits in divers with DCI. Herein we describe our experience with neurological DCI and hematocrit values in a large series of consecutively treated divers. We performed a retrospective chart review of 200 consecutive recreational divers that received treatment for DCI. Standard statistical analyses were performed to determine if there were any significant relationships between diving-related or demographic parameters, neurological manifestations, and hematocrit. In 177 of the 200 divers (88.5%), at least one manifestation of neurological DCI (mild, moderate, or severe) was present. The median hematocrit value was 43, for both male and female divers, with a range of 30 to 61. Hematocrit values did not correlate with diver age or level of diving experience. In male divers, the hematocrit did not correlate with neurological symptoms, including the sub-group with values of 48 or greater. In contrast, female divers with hematocrit values of 48 or greater were significantly more likely to develop motor weakness (p=0.002, Fisher's exact test) and an increased number of severe sensory symptoms (p=0.001, Kendall's tau statistic). Neurological complications are common in recreational divers treated for DCI. Hematocrit values of 48 or higher were correlated with the presence of motor weakness and severity of sensory symptoms in female divers. The hematocrit did not correlate with neurological DCI in male divers.
Hyperbaric oxygen therapy (HBO2T) is a specialty with wide clinical applications and study fields. An evaluation of the major research direction of HBO2T studies would be helpful for researchers in this field. In this study, we identified the most frequently cited HBO2T articles to analyze the study focus of HBO2T research in the past 10 years. "Hyperbaric oxygen" was used as the keyword to search articles in PubMed between January 2000 and November 2010. The cited times of an article were tracked in Google Scholar. The top 100 most-cited articles were identified and their publication year, author nationalities, journal, study field and style were recorded and analyzed. In total, 2,362 HBO2T-related articles were retrieved. The number of HBO2T articles published per year has been increasing during the past 10 years. More than half of the top-cited articles (52/100) were from studies in the United States. Studies focusing on stroke (20), radiation injury (11), carbon monoxide (10), and wounds (9) accounted for 50% of the top-cited articles. HBO2T has been a field of increasing scientific publications in the past 10 years. The focus of research fields were stroke, radiation injury, carbon monoxide and wounds. The United States maintains an important influence on HBO2T studies.
To analyze the studies on decompression illness (DCI) in China in the past 10 years. We searched three Chinese databases and collected studies on DCI for further analysis. On the basis of findings, we proposed the issues on DCI in China. There are more than 50,000 active divers in China, the majority of whom are fishing divers. Among them, the incidence of DCI is still at a high level because they have little or no knowledge of diving and diving medicine, the quality of diving equipment is poor, and divers generally do not follow the regulations of diving. There are few dive physicians in China, and the general clinicians have poor knowledge about, or pay little attention to, dive medicine. This might be the major cause of the poor quality of studies on DCI. There is no consensus in the classification of DCI and treatment tables for DCI treatment. These are factors affecting systemic review and further meta-analysis of available studies on DCI. It is imperative to generalize knowledge in not only divers and diving-related practitioners but general practitioners as well.
Diving is a popular recreational activity in Hong Kong, and there is an associated incidence of mortality. This individual case review of reported diving-related deaths occurring in Hong Kong waters between 2006-2009 inclusive, was conducted as part of the ongoing DAN Asia-Pacific dive fatality reporting project. The eight reported deaths involved one snorkeler and seven scuba divers. Six of the victims were male and two were female. The disabling injury in at least one death, possibly two, appeared to have been cardiac-related; two involved trauma from impact with boats; and asphyxia was believed to be the disabling injury in four or five fatalities. Two of the deaths occurred during open-water diver training and one during advanced diver training. Inexperience, pre-existing medical conditions, poor supervision, solo diving and poor sea conditions were key factors in these deaths. It is hoped that this review provides a suitable model for others to emulate in reporting dive fatalities.
Informal surveys at CME meetings have shown that approximately one-third of patients in the United States receive hyperbaric oxygen (HBO2) for delayed radiation injury. More than 600,000 patients receive radiation for malignancy in our country annually, and about one-half will be long-term survivors. Serious radiation complications occur in 5-10% of survivors. A large population of patients is therefore at risk for radiation injury. HBO2 has been applied to treat patients with radiation injury since the mid-1970s. Published results are consistently positive, but the level of evidence for individual publications is usually not high level, consisting mostly of case series and case reports. Only a rare randomized controlled trial has been accomplished. Radiation injury is one of the UHMS "approved" indications, and third-party payors will usually reimburse for this application. This updated review summarizes the publications available reporting results in treating radiation-injured patients. Mechanisms of HBO2 in radiation injury are discussed briefly. Outcome is reported on a mostly anatomic basis though due to the nature of the injury a positive outcome at one anatomic site is supportive of HBO2 at other sites. The potential benefit of prophylactic HBO2 before frank damage is also discussed in high-risk patients. The concerns of HBO2 enhancing growth of or precipitating recurrence of malignancy is discussed and largely refuted.
Pressure plotted against time after start of compression (Start: 12:25 PM). Circles identify measurements of standing steadiness. The dotted line indicates pressure changes during excursions. The lower panel shows excursion details for the bottom phase. Four divers followed profile A and the other four profile B. One from each group was excluded from analysis (see text). 
Linear Regression Coefficients of Path Length (MM) vs. Time (Days) during the Bottom Phase.
Postural sway in six divers measured 38 times on a force platform in four different test conditions during a 19-day simulated saturation dive in helium-oxygen to 240 msw. Path length, i.e. the movement of the center of pressure (in mm) during one minute of quiet standing, is plotted against time (days after start of compression). Path length values were dichotomized using the median (indicated with a thin horizontal line) as cut-point. Dots and circles indicate sway above and below median respectively. P-values are shown for the null-hypothesis that postural sway varied randomly throughout the dive (runs test). A small vertical line indicates that the measurement was performed during an excursion. Note that in cells with significant results dots occur more frequently during the bottom phase, and circles more frequently during decompression.
Mean postural sway in six divers measured 38 times on a force platform in four different test- conditions during a 19-day simulated saturation dive in helium-oxygen to 240 msw. Path length, i.e. the movement of the center of pressure (in mm) during one minute of quiet standing, is plotted against time (days after start of compression). Left panel: with subjects standing on bare platform. Right panel: standing on a 10 cm thick foam rubber mat. 
There is evidence that increased ambient pressure causes an increase in postural sway. This article documents postural sway at pressures not previously studied and discusses possible mechanisms. Eight subjects participated in a dry chamber dive to 240 msw (2.5 MPa) saturation pressure. Two subjects were excluded due to unilateral caloric weakness before the dive. Postural sway was measured on a force platform. The path length described by the center of pressure while standing quietly for 60 seconds was used as test variable. Tests were repeated 38 times in four conditions: with eyes open or closed, while standing on bare platform or on a foam rubber mat. Upon reaching 240 msw, one subject reported vertigo, disequilibrium and nausea, and in all subjects, mean postural sway increased 26% on bare platform with eyes open (p < 0.05) compared to predive values. There was no significant improvement in postural sway during the bottom phase, but a trend was seen toward improvement when the subjects were standing with eyes closed on foam rubber (p = 0.1). Postural sway returned to predive values during the decompression phase. Postural imbalance during deep diving has been explained previously as HPNS possibly including a specific effect on the vestibulo-ocular reflex. Although vertigo and imbalance are known to be related to compression rate, this study shows that there remains a measurable increase in postural sway throughout the bottom phase at 240 msw, which seems to be related to absolute pressure.
Decompression sickness (DCS) and central nervous system oxygen toxicity are inherent risks for "inside" attendants (IAs) of hyperbaric chambers. At the Hyperbaric Medicine Center at the University of California San Diego (UCSD), protocols have been developed for decompressing IAs. Protocol 1: For a total bottom time (TBT) of less than 80 minutes at 2.4 atmospheres absolute (atm abs) or shallower, the U.S. Navy (1955) no-decompression tables were utilized. Protocol 2: For a TBT between 80 and 119 minutes IAs breathed oxygen for 15 minutes prior to initiation of ascent. Protocol 3: For a TBT between 120-139 minutes IAs breathed oxygen for 30 minutes prior to ascent. These protocols have been utilized for approximately 28 years and have produced zero cases of DCS and central nervous system oxygen toxicity. These results, based upon more than 24,000 exposures, have an upper limit of risk of DCS and oxygen toxicity of 0.02806 (95% CI) using UCSD IA decompression Protocol 1, 0.00021 for Protocol 2, and 0.00549 for Protocol 3. We conclude that the utilization of this methodology may be useful at other sea-level multiplace chambers.
We investigated the effects of hyperbaric oxygen (HBO2) and/or 5-fluorouracil (5-FU) on the proliferation and metastasis of human nasopharyngeal carcinoma (NPC) cell line CNE2Z and the underlying mechanisms involved. Nasopharyngeal carcinoma (NPC) CNE2Z cells were randomly divided into four groups: Group A: control group; Group B: 5-FU group; Group C: HBO2 group; Group D: 5-FU plus HBO2 group. The inhibitory effects on CNE2Z cells proliferation in the four groups after 24, 48 and 72 hours of treatment were measured by MTT-colorimetric method. Transwell chamber assay was performed to determine the effects of HBO2 and/or 5-FU on the metastasis of CNE2Z cells; Expressions of MMP-9 and VEGF in CNE2Z cells were detected by immunocytochemical staining. A significant difference was observed in the inhibitory effects on CNE2Z cell proliferation (OD values) between the 5-FU group (Group B) and the control group (Group A) after 24, 48, and 72 hours of treatment (p<0.01); between the HBO2 group (group C) and the control group (Group A) after 48 and 72 hours of treatment (p<0.01); and between the HBO2 plus 5-FU group (Group D) and the control group (Group A) as well as the HBO2 plus 5-FU group (Group D) and the HBO2 group (Group C) after 24, 48, and 72 hours of treatment (p<0.01). But a significant difference between the HBO2 plus 5-FU group (Group D) and the 5-FU group (Group B) was observed only after 48 hours of treatment (p=0.030). As for metastasis, as well as MMP-9 and VEGF expression OD values, significant difference was observed between the 5-FU group (Group B) and the control group (Group A) with p<0.05, but not between the HBO2 group (Group C) and the control group (Group A). Although effects on metastasis as well as MMP-9 and VEGF expression OD values were significantly different between the 5-FU plus HBO group (group D) and group A (p<0.01), no difference was observed between Group D and Group B as well as Group D and Group C. Simple HBO2 treatment after 48 and 72 hours could inhibit the proliferation of nasopharyngeal carcinoma CNE2Z cells. The combination of HBO2 with 5-FU exhibited significant synergism in the suppression of NE2Z cell proliferation only after 48 hours of treatment compared to 5-FU. Simple HBO2 treatment could not reduce the high expressions of MMP-9 and VEGF and inhibit the metastasis of human NPC CNE2Z cells, and no synergistic effect was observed for the combination of HBO2 with 5-FU compared to 5-FU alone.
To determine the influence of a saturation dive on cardiac function, Doppler-echocardiographic measurements were compared at sea level and during a 36 atm (3,650 kPa) He-O2 dive (gas density: 7 g/liter) in four healthy men. Left ventricular systolic function was studied from time motion measurements. Transmitral flow (E:A ratio) and isovolumetric relaxation time were used to assess left ventricular diastolic function. Cardiac output was derived from systolic pulmonary and aortic valvular flows. Cardiac output decreased 4.4 +/- 0.8 vs. 5.9 +/- 1.2 liter/min at sea level) whereas stroke volume, left ventricular ejection fraction, atria and ventricular diameters remained unchanged. Thus, the decrease in cardiac output was attributed to bradycardia (56 +/- 8 vs. 73 +/- 9 beats/min at sea level) which probably resulted from the slight hyperoxia (PI(O2), 0.4 atm). We found no evidence of left ventricular diastolic dysfunction. nor did we find valvular regurgitation or pulmonary hypertension. We conclude that Doppler-echocardiography can be used safely to investigate cardiac function during human saturation dives. Our results suggest that a 36 atm He-O2 dive does not modify cardiac or systolic and diastolic function except for a slight decrease in cardiac output correlated to bradycardia.
Unlabelled: Recreational divers are introducing "deep stops" at half the depth (HD-DS) to reduce the risk of spinal DCS with only Doppler evidence to support it. Therefore this research was designed to show the effect of an HD-DS on spinal DCS manifestations by evaluating whether: (1) air diving-induced spinal DCS could be produced in awake, freely moving rats at 3.5-6.0 atm abs (350-600 kPa); and (2) whether the introduction of an HD-DS reduced spinal DCS in such a model. Fifty-one female, Wistar rats (221 to 450 g) underwent one-hour compression at 350 to 600 kPa with seven minutes of decompression with/without a five-minute DS (HD-DS / No-DS). Animals were observed for three hours. Outcomes were classified as: (1) asymptomatic; (2) breathing difficulties; (3) paralysis/weakness; (4) immobility; or (5) death. Eight animals, exposed to 385 kPa air breathing for 60 minutes followed by a three-staged decompression of 7.5 minutes, remained asymptomatic. The profile is known to produce spinal DCS in anesthetized rats. Eleven animals were then used to determine the threshold for DCS: 500 kPa. A total of 14 animals were compressed to 550 kPa (Group 1). Group 1-A (n = 8) No-DS; Group 1-B (n = 6) HD-DS; 18 were compressed to 600 kPa (Group 2). Group 2-A (n = 8) No-DS; Group 2-B (n = 10) HD-DS. Results: (1) 385 kPa protocol did not produce visible DCS manifestations in awake rats. The binomial probability of no DCS in this sample size is 0.002818 for the proportion expected from a published report. The binomial probability of no fatalities is 0.005346). (2) No animals developed spinal DCS when assessed by visible paralysis/weakness or immobility, so no difference could be shown. Group 1-A: two deaths; two breathing abnormalities; four asymptomatic. Group 1-B: all asymptomatic. Difference recorded for breathing difficulties (p = 0.0483); none for fatalities (p = 0.2024). Group 2 mortality was 55% (n = 10). Group 2-A and 2-B: no difference for death (p = 0.6063) or breathing problems (p = 0.2084). Conclusions: This model could not evaluate HD-DS for the prevention of spinal DCS in rats.
The hyperbaric environment causes a sustained diuresis accompanied by normal water intake and a decrease in insensible water loss. The maintained water intake may be necessary for the maintenance of water balance because of a reduced ability of the kidney to retain water, or may be causal in the diuresis. This problem was studied in four male subjects. Each ingested 1 liter of water (15 degrees C) at 0800 and 2000 h on different days, at 1 atm abs during a predive control, at 31 atm abs, and at 1 atm abs during the postdive control period. Urine was collected 30 min before and 3 h after the drink. Plasma vasopressin (VP) showed a circadian rhythm only at 1 atm abs, higher during the daytime. Because of this, and slightly lower VP levels at hyperbaria, a decrease in VP in response to the water load was significantly detectable only at 1 atm abs during the daytime. At 60 min after all water loads, there were no differences in plasma VP or plasma or urinary osmolality. Variability in the length of time of similarly reduced urine osmolality and increased free water excretion accounted for the increased urine flow during day compared to night (P < 0.05) at 120 and 150 min after the water load. The ability to excrete a water load both day (free water clear-ance, P < 0.05 at 60 min post-drink) and night (free water clearance, P < 0.05 at 60, 90, and 120 min post-drink) at 31 atm abs was enhanced. It is concluded that maintained water intake at hyperbaria is necessary to maintain water balance because there is a reduced ability of the body through renal mechanisms to retain a water load.
Individual values for the change in diffusing capacity post-intervention.
Age, anthropometric data and baseline pulmonary function for the ten subjects included in the study. Male Female Total
Mean diffusing capacity values for control and experimental conditions at various time points.
The purpose of this study was to assess the contribution of SCUBA to the pulmonary effects of diving to 4.5 meters depth in healthy subjects using a randomized crossover control condition. Ten healthy divers performed two 60-minute 'dives' using SCUBA in a swimming pool. The non-immersed 1 ATA SCUBA control exposure took place at ambient pressure in the laboratory. Thirty minutes prior to, and 30 and 90 minutes post-exposure, FVC (forced vital capacity), FEV1.0 (forced expired volume), peak expiratory flow rate (PEFR), diffusing capacity (DL(co)), heart rate (HR) and temperature were measured. No significant differences were noted in HR, temperature or spirometry between the two conditions. A significant reduction in diffusing capacity occurred at 30 and 90 minutes after the pool dive (9.3% and 15.1%, respectively, p < 0.05). There was no concordant change in DL(co) following the non-immersed 1 ATA SCUBA control. Thus, a pool dive to 4.5 meters for 60 minutes causes a decrease in DL(co), without a change in spirometry, while breathing from SCUBA equipment without immersion causes no significant change in lung function.
When divers are exposed to extreme atmospheric pressures they may exhibit symptoms of the high pressure nervous syndrome (HPNS). Although clinical HPNS symptoms are well described, little is known about the underlying pathophysiologic mechanisms. Special HPNS signs like vertigo and tremor suggested sensory-motor hyperexcitability resulting from brainstem dysfunction. We therefore studied brainstem auditory evoked potential (BAEP) repeatedly in four divers during an experimental deep helium-oxygen saturation dive to 450 meters of seawater (msw). Wave I (auditory nerve response) latency decreased whereas interpeak latencies (IPLs) I-III and I-V, which indicate respective cochleo-pontine and cochleo-mesencephalic transmission time, prolonged during the dive. IPLs III-V also prolonged the dive, but with greater variability among divers. Two divers showed a marked reversal of the normal attenuation effect of increased stimulus presentation rates on IV and V amplitudes during compression, an effect that subsided during the stay at bottom depth. This finding might indicate a relative enhancement of synaptic excitability and is presumed to be a feature of HPNS. Wave I latency reduction might at least partly be caused by accelerated sound conduction in dense helium. Additionally, an upward shift of middle ear resonance frequencies in helium can induce a basal shift of the main cochlear portion responding to the wide band clicks. This effect may reduce wave I latency due to greater relative input from the basal high frequency-short latency-cochlear neurons. Pressure-induced decrease of nerve conduction velocity, delay of synaptic transmission, and inhibitory modulation of midbrain auditory afferents possibly contributed to observed interpeak latency prolongations. Clinical HPNS signs, such as tiredness, dizziness, postural and intentional hand tremor, ataxia, and opsoclonus, were noted in three divers after reaching 300 msw and continued throughout the 37-h stay at bottom depth.
We evaluated CO2 retention in 24 Navy construction divers breathing air at 1 atm abs (101.3 kPa) and 40% O2 (40/60) nitrox at 4 atm abs (Po2 of 162.1 kPa) inside a pressure chamber. The divers sat immersed to the sternal notch and exercised against pneumatically loaded pedals at a Vo2 of approximately 1.3 liter/min. The mean end-tidal CO2 tension (PET(CO2)2) at 1 atm abs (45.7 +/- 5.0 SD torr) was significantly higher than that of non-divers and diving trainees (40 +/- 5.0) but did not increase significantly at depth (47.1 +/- 6.3). The ranking of CO2 retention was not maintained at depth. Unpredictable upward and downward shifts of up to 10 torr occurred in some divers. The PET(CO2) of six of the divers at pressure was greater than 50 torr, which based on animal studies markedly increases the risk of central nervous system oxygen toxicity. We translated their values into individual depth limits with 40/60 nitrox: three with 50 < PET(CO2) < 55 torr were forbidden to dive beyond 25 m and three with values > 55 torr were restricted to 20 m. We propose that whenever possible, PET(CO2) during exercise at pressure be measured in potential nitrox users and that the above PO2 limits be enforced on moderate and extreme CO2 retainers, respectively.
For non-hyperbaric purposes, the Baxter Flo-Gard 6201 volumetric pump is capable of infusing multiple types of fluids at rates of 1-1,999 ml x h(-1). We designed a study to determine flow accuracy of this pump at variable rates, fluid viscosities, and volumes over a range of chamber pressures. For hyperbaric use, the pump pressure sensor was adjusted. Sodium chloride solution 0.9% (NS), enteral formula, and packed red blood cells (PRBC) were infused at varying rates from 86.1 to 304 kPa (0.85 to 3.0 atm abs). For NS, measured compared to set flow rates ranged from 12.5% to -7.5% at settings of 1 and 5 ml x h(-1) from 86.1 to 304 kPa (0.85 to 3.0 atm abs) pressures, respectively. For NS infusions at a set rate of 100 ml x h(-1), the measured flow was identical to the set rate at all pressures. At flow settings of 1,999 ml x h(-1), the measured flow varied from the set flow by +/-4.9% Enteral infusion at 100 ml x h(-1) showed approximately a 3% increase in the measured vs. set flow rate. PRBC measured flow rates ranged from -0.4 to 6% of the set rate. During chamber compression and decompression, with set flow rates from 1 to 10 ml x h(-1), the measured flow was considerably less than expected during compression and more than expected during decompression. In conclusion, the Baxter Flo-Gard 6201 infusion pump demonstrated acceptable performance for infusing saline, enteral formula, and PRBC at low and high infusion rates into the pressurized monoplace hyperbaric chamber up to 304 kPa (3 atm abs), with the exception of low rates during compression and decompression.
Treatment with the surface-active agent Pluronic F-68, shown to modulate the hemodynamic effects of venous air emboli (VAE) in dogs, may be useful for treatment of VAE in divers. We report on the effects of injections of Pluronic F-68 on responses to continuous air infusion in swine. Pretreatment made no significant difference in any hemodynamic or ventilatory variables, but the rise of pulmonary vascular resistance caused by air infusion was greater in surfactant-treated animals; this was also evident after a second treatment during the air infusion. The small effect of surfactant treatment in our study on swine contrasts the effects reported previously in dogs, and could be due to species-specific differences in lung physiology-anatomy, or due to difference in experimental design. We speculate that the minor changes we observed were caused by deeper penetration of the bubbles into the pulmonary arterial tree after surfactant treatment.
Electrocardiogram (ECG) analysis was performed in three human divers during a 71 atm (7,200 kPa) saturation dive (COMEX HYDRA 10 experiment). The inhaled gas mixture was slightly hyperoxic; its composition was basically helium and oxygen. Hydrogen was introduced during compression and its partial pressure reached 20 atm. ECG changes were the same in the three divers. Marked bradycardia rapidly appeared at the beginning of compression, then this response adapted throughout the dive. P-R, QRS, and Q-T intervals and the S-T segment did not change significantly. The QRS axis remained stable. However, a rightward shift occurred in P and T vector angles. These changes were correlated with time and gas density, respectively. The modifications of ventricular repolarization during compression are similar to those we observed during the HYDRA 9 COMEX dive. They may correspond to changes in duration of myocardial cell repolarization due to increased intrathoracic pressure changes with dense-gas breathing. A marked global diminution of voltage occurred during the decompression period. This suggests that accumulation of micro bubbles in tissues may influence the impedance, causing an artifact in the amplitude of ECG complexes.
Fire can be catastrophic in the confined space of a hyperbaric chamber. From 1923 to 1996, 77 human fatalities occurred in 35 hyperbaric chamber fires, three human fatalities in a pressurized Apollo Command Module, and two human fatalities in three hypobaric chamber fires reported in Asia, Europe, and North America. Two fires occurred in diving bells, eight occurred in recompression (or decompression) chambers, and 25 occurred in clinical hyperbaric chambers. No fire fatalities were reported in the clinical hyperbaric chambers of North America. Chamber fires before 1980 were principally caused by electrical ignition. Since 1980, chamber fires have been primarily caused by prohibited sources of ignition that an occupant carried inside the chamber. Each fatal chamber fire has occurred in an enriched oxygen atmosphere (> 28% oxygen) and in the presence of abundant burnable material. Chambers pressurized with air (< 23.5% oxygen) had the only survivors. Information in this report was obtained from the literature and from the Undersea and Hyperbaric Medical Society's Chamber Experience and Mishap Database. This epidemiologic review focuses on information learned from critical analyses of chamber fires and how it can be applied to safe operation of hypobaric and hyperbaric chambers.
We studied the effect of SF6-O2 breathing on air bubbles injected into skeletal muscle, rat-tail tendon, the anterior chamber of the eye, and spinal white matter. Decompression-induced nitrogen bubbles in adipose tissue were studied during breathing of SF6-O2 (80/20). The results of SF6-O2 breathing are compared with previous experiments using heliox (80/20) as the breathing medium. Bubbles studied in skeletal muscle, eye chamber, and spinal white matter were found to behave in a two-phased manner during SF6-O2 (80/20) breathing. All bubbles would initially decrease rapidly in size for a period of 10-80 min (depending on the tissue). Subsequently, the bubbles stabilized and decreased in size with a shrinking rate near zero. In spinal white matter, very small bubbles decreased size with a shrinking rate near zero. In spinal white matter, very small bubbles could disappear before development of the slow phase. All bubbles in tendon shrank at a rather constant rate during SF6-O2 (80/20) breathing until they disappeared. During SF6-O2 (80/20) breathing, all bubbles in adipose tissue shrank and disappeared at least as fast as during heliox (80/20) breathing. Just before disappearance of the bubbles the shrinking rate slowed. Comparison of the effects of SF6-O2 (80/20) and heliox (80/20) breathing suggests that countercurrent gas exchange is at work in some tissues.
After the crash of TWA flight 800, U.S. Navy (USN) and civilian divers recovered the aircraft and the victims' remains from 117 feet of sea water (fsw). Safety information was gathered from observations, interviews, and medical and diving records. Of 752 dives employing surface decompression using oxygen (SDO2), 10 divers required recompression treatments, mainly for type 2 decompression sickness (DCS). When using hot water heating, the DCS risk was high until the dive profiles were modified. Divers made nearly 4,000 no-decompression scuba dives. In eight scuba divers and one tender treated with recompression, the diagnoses included DCS (3), arterial gas embolism (AGE) (1), and vascular headache (2). All USN divers recovered fully. The experience is consistent with previous work suggesting an increase in DCS risk in warmer SDO2 divers. The USN SDO2 tables can be made safer by limiting bottom time and extending decompression. Even under stressful conditions, rapid ascents resulting in AGE are uncommon. Vascular headaches can mimic DCS by responding to oxygen.
In our previous research, a deep 5-min stop at 15 msw (50 fsw), in addition to the typical 3-5 min shallow stop, significantly reduced precordial Doppler detectable bubbles (PDDB) and "fast" tissue compartment gas tensions during decompression from a 25 msw (82 fsw) dive; the optimal ascent rate was 10 msw (30 fsw/min). Since publication of these results, several recreational diving agencies have recommended empirical stop times shorter than the 5 min stops that we used, stops of as little as 1 min (deep) and 2 min (shallow). In our present study, we clarified the optimal time for stops by measuring PDDB with several combinations of deep and shallow stop times following single and repetitive open-water dives to 25 msw (82 fsw) for 25 mins and 20 minutes respectively; ascent rate was 10 msw/min (33 fsw). Among 15 profiles, stop time ranged from 1 to 10 min for both the deep stops (15 msw/50 fsw) and the shallow stops (6 msw/20 fsw). Dives with 2 1/2 min deep stops yielded the lowest PDDB scores--shorter or longer deep stops were less effective in reducing PDDB. The results confirm that a deep stop of 1 min is too short--it produced the highest PDDB scores of all the dives. We also evaluated shallow stop times of 5, 4, 3, 2 and 1 min while keeping a fixed time of 2.5 min for the deep stop; increased times up to 10 min at the shallow stop did not further reduce PDDB. While our findings cannot be extrapolated beyond these dive profiles without further study, we recommend a deep stop of at least 2 1/2 mins at 15 msw (50 fsw) in addition to the customary 6 msw (20 fsw) for 3-5 mins for 25 meter dives of 20 to 25 minutes to reduce PDDB.
-Matrix of Experimental Dive Profiles
-Fast tissue saturation and bubble scores after the different dive profiles
-Incidence of Doppler detected bubbles after the different dive profiles
Ascent Rate vs. % high & very high bubble grades for all profiles 
Percentage high and very high bubble grades versus stops (all ascent rates) 
In spite of many modifications to decompression algorithms, the incidence of decompression sickness (DCS) in scuba divers has changed very little. The success of stage, compared to linear ascents, is well described yet theoretical changes in decompression ratios have diminished the importance of fast tissue gas tensions as critical for bubble generation. The most serious signs and symptoms of DCS involve the spinal cord, with a tissue half time of only 12.5 minutes. It is proposed that present decompression schedules do not permit sufficient gas elimination from such fast tissues, resulting in bubble formation. Further, it is hypothesized that introduction of a deep stop will significantly reduce fast tissue bubble formation and neurological DCS risk. A total of 181 dives were made to 82 fsw (25 m) by 22 volunteers. Two dives of 25 min and 20 min were made, with a 3 hr 30 min surface interval and according to 8 different ascent protocols. Ascent rates of 10, 33 or 60 fsw/min (3, 10, 18 m/min) were combined with no stops or a shallow stop at 20 fsw (6 m) or a deep stop at 50 fsw (15 m) and a shallow at 20 fsw (6 m). The highest bubbles scores (8.78/9.97), using the Spencer Scale (SS) and Extended Spencer Scale (ESS) respectively, were with the slowest ascent rate. This also showed the highest 5 min and 10 min tissue loads of 48% and 75%. The lowest bubble scores (1.79/2.50) were with an ascent rate of 33 fsw (10 m/min) and stops for 5 min at 50 fsw (15 m) and 20 fsw (6 m). This also showed the lowest 5 and 10 min tissue loads at 25% and 52% respectively. Thus, introduction of a deep stop significantly reduced Doppler detected bubbles together with tissue gas tensions in the 5 and 10 min tissues, which has implications for reducing the incidence of neurological DCS in divers.
Radiation therapy is often utilized as adjunctive or primary treatment for malignancies of the abdomen and pelvis. Radiation complications are infrequent, but can be life threatening or significantly diminish the quality of life. Radiation necrosis is an approved indication for hyperbaric oxygen (HBO2). Previous publications have reported results in treating delayed radiation injuries involving many sites. This paper reports the experience of a single physician group in treating delayed injuries of the abdomen and/or pelvis. Forty-four such patients have been treated since 1979. Of the 41 patients available for follow up, 26 have healed; 6 failed to heal; and 9 patients had an inadequate course of therapy (fewer than 20 treatments). Especially encouraging was the resolution of fistulae in six of eight patients with only three requiring surgery for closure. Overall, the success rate in patients receiving at least 20 HBO2 treatments was 81%. Hyperbaric oxygen is a useful adjunct in treatment of delayed radiation injuries of the pelvis and abdomen.
A 29-year-old man was brought to an emergency department by the United States Coast Guard with chief complaints of severe abdominal pain, right leg paresthesia and weakness following four deep air dives. Physical examination before recompression treatment was remarkable for diffuse abdominal tenderness and right leg weakness. The patient was diagnosed in the emergency room with type II decompression sickness (DCS) and underwent standard recompression therapy. He experienced complete resolution of weakness after hyperbaric oxygen (HBO) therapy, but his abdominal pain was persistent. Further investigation led to the diagnosis of acute appendicitis with perforation. The patient underwent appendectomy and intravenous antibiotic therapy and was discharged to his home on hospital day five without complications. This case reinforces the importance of careful clinical assessment of divers and illustrates the potentially wide differential diagnosis of DCS. This is the first reported case of recompression treatment of a diver with acute appendicitis and type II DCS.
Top-cited authors
Neil B Hampson
  • Virginia Mason Medical Center
John J Feldmeier
  • University of Toledo
Alf O Brubakk
  • Norwegian University of Science and Technology
Claude A Piantadosi
  • Duke University Medical Center
Richard Vann
  • Duke University