Estimated workload intensity during volunteer aquarium dives.

BACKGROUND: This study aimed to characterize the physiological demands of working dives on volunteer divers at a public aquarium in the USA. AIMS: To estimate the workloads associated with volunteer dives in a US aquarium. METHODS: Participants completed a medical and diving history questionnaire. Measurements included blood pressure before and after diving and continuous ECG (Holter) monitoring during diving. Dive profiles were recorded using loggers. Mean workload was estimated from total air consumption. RESULTS: Twenty-seven divers recorded 49 air dives over 5 days. Two-thirds were male and ages ranged from 40 to 78 years. Typically, each diver made two dives with a 30-60 min surface interval. Mean heart rate while diving was 100 beats per minute (bpm). Mean estimated workload during the dives recorded during this study was 5.8 metabolic equivalents (METS), with a range from 4.1 to 10.5. The highest mean recorded heart rate was 120 bpm over 40 min, vacuuming the floor in the shark exhibit. CONCLUSIONS: Given the mean age of this sample and the prevalence of cardiovascular risk factors (body mass index, high cholesterol and hypertension), it may be prudent for aquariums to regularly monitor SAC/kg and heart rate in volunteer divers, to identify which tasks require the highest workload intensity. Divers with existing cardiovascular risk factors might then be employed in dives with lighter workloads. In conclusion, volunteer dives at this aquarium required a mean workload intensity that was described by recreational divers as moderate. The highest workload, at 10 METS for 23 min, would be considered by many recreational divers as exhausting.

Epidemiology of morbidity and mortality in US and Canadian recreational scuba diving.

OBJECTIVES: This study investigates morbidity and mortality suffered by divers in the USA and Canada. STUDY DESIGN: Prospectively recruited probability-weighted sample for estimating the national burden of injury and a weighted retrospective survey for estimating exposure. METHODS: The National Electronic Surveillance System and Canadian Hospitals Injury Reporting and Prevention Program (CHIRPP) were searched for scuba diving injuries. The Divers Alert Network diving fatality database was searched for deaths, and Sports and Fitness Industry Association estimates for diving were obtained from annual surveys. RESULTS: In the USA, there were an estimated 1394 emergency department (ED) presentations annually for scuba-related injuries. The majority (80%) were treated and/or released. There were an estimated 306 million dives made by the US residents 2006-2015 and concurrently 563 recreational diving deaths, a fatality rate of 0.18 per 105 dives and 1.8 per 105 diver-years. There were 658 diving deaths in the US 2006-2015 and 13,943 ED presentations for scuba injuries, giving a ratio of 47 diving deaths in the USA for every 1000 ED presentations. There were 98 cases of scuba-related injuries identified in the CHIRPP data. The prevalence of scuba-related injuries for patients aged 3-17 years was 1.5 per 105 cases, and the prevalence of scuba-related injuries to patients 18-62 years was 16.5 per 105 cases. DISCUSSION: In Canada and the USA, only one out of every 10,000 ED presentations is due to a scuba-related injury. That there are 47 deaths for every 1000 ED presentations for scuba injuries speaks to the relatively unforgiving environment in which scuba diving takes place. For 1.8 deaths per million recreational dives, mortality in scuba diving is nonetheless relatively low.

Possible central nervous system oxygen toxicity seizures among US recreational air or enriched air nitrox open circuit diving fatalities 2004-2013.

BACKGROUND: The first diver certification programme for recreational 'enriched air nitrox' (EAN) diving was released in 1985. Concerns were expressed that many EAN divers might suffer central nervous system (CNS) oxygen toxicity seizures and drown. METHODS: US fatalities on open-circuit scuba occurring between 2004-2013, where the breathing gas was either air or EAN, were identified. Causes of death and preceding circumstances were examined by a medical examiner experienced in diving autopsies. Case notes were searched for witnessed seizures at elevated partial pressures of oxygen. RESULTS: The dataset comprised 344 air divers (86%) and 55 divers breathing EAN (14%). EAN divers' fatal dives were deeper than air divers' (28 msw vs 18 msw, p < 0.0001). Despite this, of the 249 cases where a cause of death was established, only three EAN divers were considered to have possibly died following CNS oxygen toxicity seizures at depth (ppO2 132, 142 and 193 kPa). CONCLUSION: The analysis of recreational diving fatalities in the US over 10 years found just one death likely from CNS oxygen toxicity among EAN divers. A further two possible, although unlikely, cases were also found. Fears of commonplace CNS oxygen toxicity seizures while EAN diving have not apparently been realized.

Influence of repeated daily diving on decompression stress.

Acclimatization (an adaptive change in response to repeated environmental exposure) to diving could reduce decompression stress. A decrease in post-dive circulating venous gas emboli (VGE or bubbles) would represent positive acclimatization. The purpose of this study was to determine whether four days of daily diving alter post-dive bubble grades. 16 male divers performed identical no-decompression air dives on 4 consecutive days to 18 meters of sea water for 47 min bottom times. VGE monitoring was performed with transthoracic echocardiography every 20 min for 120 min post-dive. Completion of identical daily dives resulted in progressively decreasing odds (or logit risk) of having relatively higher grade bubbles on consecutive days. The odds on Day 4 were half that of Day 1 (OR 0.50, 95% CI: 0.34, 0.73). The odds ratio for a >III bubble grade on Day 4 was 0.37 (95% CI: 0.20, 0.70) when compared to Day 1. The current study indicates that repetitive daily diving may reduce bubble formation, representing a positive (protective) acclimatization to diving. Further work is required to evaluate the impact of additional days of diving and multiple dive days and to determine if the effect is sufficient to alter the absolute risk of decompression sickness.

Venous gas bubble formation and decompression risk after scuba diving in persons with chronic spinal cord injury and able-bodied controls.

STUDY DESIGN: Prospective study. OBJECTIVE: To evaluate the formation of venous gas bubbles following open-sea scuba dives in persons with chronic spinal cord injury (SCI) and in able-bodied diving instructors (C) and to assess the risk for decompression sickness (DCS). SETTING: Field study at the Island of Krk, Croatia. METHODS: Gas bubbles were monitored with an ultrasound scanner 40 min after surfacing. The probability of DCS (P((DCS))) was estimated from the recorded depth-time profile using a decompression model. RESULTS: Divers completed six dives in 3 days using a modified Bühlmann decompression model, and none developed signs of DCS. Mean P((DCS)) was similar in both groups, SCI (0.51+/-0.2%) and C (0.64+/-0.27%), and was seen to increase with subsequent dives. Number of bubbles (bubbles per cm(2)) was low in both groups on all 3 days of diving. CONCLUSIONS: We have used the P((DCS)) as a severity index of diving exposure. Overall, the severity of exposure in SCI subjects was consistent with the range of typical recreational dives, suggesting that the diving profile used is very safe.

Common causes of open-circuit recreational diving fatalities.

Diving fatalities causes were investigated in 947 recreational open-circuit scuba diving deaths from 1992-2003. Where possible, cases were classified at each step of a four step sequence: trigger, disabling agent, disabling injury, cause of death (COD). The most frequent adverse events within each step were: (a) triggers 41% insufficient gas, 20% entrapment, 15% equipment problems; (b) disabling agents--55% emergency ascent, 27% insufficient gas, 13% buoyancy trouble; (c) disabling injuries--33% asphyxia, 29% arterial gas embolism (AGE), 26% cardiac incidents; and (d) COD--70% drowning, 14% AGE, 13% cardiac incidents. We concluded that disabling injuries were more relevant than COD as drowning was often secondary to a disabling injury. Frequencies and/ or associations with risk factors were investigated for each disabling injury by logistic regression. (The reference group for each injury was all other injuries.) Frequencies and/or associations included: (a) asphyxia--40% entrapment (Odds Ratio, OR > or = 30), 32% insufficient gas (OR = 15.9), 17% buoyancy trouble, 15% equipment trouble (OR = 4.5), 11% rough water, drysuit (OR = 4.1), female gender (OR = 2.1); (b) AGE--96% emergency ascent (OR > or = 30), 63% insufficient gas, 17% equipment trouble, 9% entrapment; (c) cardiac incidents--cardiovascular disease (OR = 10.5), age > 40 (OR = 5.9). Minimizing the frequent adverse events would have the greatest impact on reducing diving deaths.

Influence of bottom time on preflight surface intervals before flying after diving.

Previous trials of flying at 8,000 ft after a single 60 fsw, 55 min no-stop air dive found low decompression sickness (DCS) risk for a 11:00 preflight surface interval (PFSI). Repetitive 60 fsw no-stop dives with 75 and 95 min total bottom times found 16:00. Trials reported here investigated PFSIs for a 60 fsw, 40 min no-stop dive and a 60 fsw, 120 min decompression dive. The 40 min trials began with a 12:05 PFSI (USN guideline) which was incrementally reduced to 0:05 (three DCS incidents in 281 trials). The 120 min trials began with a 22:46 PFSI (USN guideline) which was reduced to 2:00 (nine incidents in 281 trials); 2:00 was rejected with six incidents. Low-risk PFSIs for the 40 min dive were nearly 12 hours shorter than for the 55 min dive, and low-risk PFSIs for the single 120 min decompression dive were 12 hours shorter than for the 75-95 min repetitive dives. With the dry, resting conditions of these dives, low-risk PFSIs appeared to be sensitive to dive profile characteristics such as bottom time, repetitive diving, and decompression stops. Whether this is so for wet, working dives is unknown.

First aid normobaric oxygen for the treatment of recreational diving injuries.

INTRODUCTION: First aid oxygen (FAO2) has been widely used as an emergency treatment for diving injuries, but there are few studies supporting its efficacy. METHODS: 2,231 sequential diving injury reports collected by the Divers Alert Network (DAN) Injury database from 1998 to 2003 were examined. RESULTS: 47% (1,045) of cases received FAO2. The median time to FAO2 treatment after surfacing was four hours and after symptom onset was 2.2 hours. Persistent complete relief (14%) or improvement (51%) was seen with FAO2 alone (65% overall response; n = 330). After one recompression treatment 67% of FAO2 patients reported complete relief compared to 58% of the no FAO2 group (OR = 1.5, 95% CI = 1.2 -1.8). FAO2 given at any time after surfacing significantly reduced the odds of multiple recompression treatments (OR = 0.83, 0.70-0.98). When FAO2 was given within 4 hours of surfacing, the OR decreased to 0.50 (0.36-0.69) yielding a number needed to treat of 6. Case severity affected urgency of FAO2 treatment. Individuals with more prominent symptoms received prompt treatment. Cardiopulmonary, skin, and serious neurological symptoms had shorter delays to FAO2 (p < 0.001). CONCLUSIONS: FAO2 increased recompression efficacy and decreased the number of recompression treatments required if given within four hours after surfacing.

Diving behaviour and decompression sickness among Galapagos underwater harvesters.

Diving conditions, dive profiles, vascular bubbles, and symptoms of decompression sickness (DCS) in a group of Galapagos commercial divers are described. They harvest sea cucumbers from small boats with surface supplied air (hookah). Dive profiles for 12 divers were recorded using dive loggers, and bubble formation was measured in the pulmonary artery. DCS symptoms were assessed by interview. A total of 380 immersions were recorded over a nine day period. The divers did on average 6.3 immersions per day, in a yo-yo pattern. Mean overall depth was 34.5 FSW. Maximum recorded depth was 107 FSW. Average bottom time per day per diver was 175 minutes. 82 % of all ascents exceeded the recommended maximum ascent rate of 30 FSW/ min. High bubble grades were observed on six occasions, but the test was unreliable. Muscle and joint pain was reported on five occasions, in three different divers. Symptoms were typically managed by analgesics, in-water recompression or not at all. The divers were extremely reluctant to seek professional help for DCS symptoms, mostly due to the high costs of treatment. We conclude that the fishermen dive beyond standard no-decompression limits, and that DCS symptoms are common.

Experimental trials to assess the risks of decompression sickness in flying after diving.

We conducted experimental trials of flying after diving using profiles near the no-decompression exposure limits for recreational diving. The objective was to determine the dependence of DCS occurrence during or after flight on the length of the preflight surface intervals (PFSI). One to three dives were conducted during a single day with dry, resting subjects in a hyperbaric chamber at depths of 40, 60, or 100 fsw (224, 286, 408 kPa). The dives were followed by PFSI of 3 to 17 hrs and a four-hour altitude exposure at 8,000 ft (75 kPa), the maximum permitted cabin altitude for pressurized commercial aircraft. Forty DCS incidents occurred during or after flight in 802 exposures of 495 subjects. The DCS incidence decreased as PFSI increased, and repetitive dives generally required longer PFSI to achieve low incidence than did single dives (p = 0.0159). No DCS occurred in 52 trials of a 17 hr PFSI, the longest PFSI tested. The results provide empirical information for formulating guidelines for flying in commercial aircraft after recreational diving.

The relative risk of decompression sickness during and after air travel following diving.

BACKGROUND: Decompression sickness (DCS) can be provoked by post-dive flying but few data exist to quantify the risk of different post-dive, preflight surface intervals (PFSI). METHODS: We conducted a case-control study using field data from the Divers Alert Network to evaluate the relative risk of DCS from flying after diving. The PFSI and the maximum depths on the last day of diving (MDLD) were analyzed from 627 recreational dive profiles. The data were divided into quartiles based on surface interval and depth. Injured divers (cases) and uninjured divers (controls) were compared using logistic regression to determine the association of DCS with time and depth while controlling for diver and dive profiles characteristics. These included PFSI, MDLD, gender, height, weight, age, and days of diving. RESULTS: The means (+/-SD) for cases and controls were as follows: PFSI, 20.7 +/- 9.6 h vs. 27.1 +/- 6.7 h; MDLD, 22.5 +/- 14 meters sea water (msw) vs. 19 +/- 11.3 msw; male gender, 60% vs. 70%; weight, 75.8 +/- 18 kg vs. 77.6 +/- 16 kg; height, 173 +/- 16 cm vs. 177 +/- 9 cm; age, 36.8 +/- 10 yr vs. 42.9 +/- 11 yr; diving > or = 3 d, 58% vs. 97%. Relative to flying > 28 h after diving, the odds of DCS (95% CI) were: 1.02 (0.61, 1.7) 24-28 h; 1.84 (1.0, 3.3) 20-24 h; and 8.5 (3.85, 18.9) < 20 h. Relative to a depth of < 14.7 msw, the odds of DCS (95% CI) were: 1.2 (0.6, 1.7) 14.7-18.5 msw; 2.9 (1.65, 5.3) 18.5-26 msw; and 5.5 (2.96, 1 0.0) > 26 msw. CONCLUSIONS: Odds ratios approximate relative risk in rare diseases such as DCS. This study demonstrated an increase in relative risk from flying after diving following shorter PFSIs and/or greater dive depths on the last day. The relative risk increases geometrically as the PFSI becomes smaller.

Hyperbaric oxygen as a therapy of Bell's palsy.

The purpose of this study was to compare the therapeutic effects of hyperbaric oxygen (HBO2) to the effects of prednisone treatment in 79 subjects with Bell's palsy. Patients were randomly assigned either to the HBO2-treated group (n = 42) or to the prednisone-treated group (n = 37). The HBO2 group was exposed to 2.8 atm abs of 100% oxygen for 60 min, twice a day, 5 days a week and was given a placebo orally. The prednisone group was exposed to 2.8 atm abs of 7% O2 (equivalent to 21% O2 in air at normal pressure) following the same schedule as the HBO2 group; prednisone was given orally (total of 450 mg in 8 days). Subjects from both groups were treated in the hyperbaric chamber for up to 30 sessions or to complete recovery, and were followed up for 9 mo. At the end of the follow-up period, 95.2% of subjects treated with HBO2, and 75.7% of subjects treated with prednisone recovered completely. The average time to complete the recovery in the HBO2 group was 22 days as opposed to 34.4 days in the control group (P < 0.001). In the HBO2-treated group, at the beginning, the altered nerve excitability test (NET) was abnormal in five subjects; three of them had normal NET by the end of the follow-up period. In the prednisone group the NET was abnormal in nine subjects at the beginning and they had not recovered by the end of the follow-up (P < 0.05). Our results suggest that HBO2 is more effective than prednisone in treatment of Bell's palsy.

Flying after diving and decompression sickness.

Reports of 1,159 decompression sickness (DCS) incidents during recreational diving were analyzed by logistic regression for the effects of flying on the occurrence of Type II DCS, complete relief of symptoms after one recompression, and residual symptoms 3 months after treatment. The relevant diver populations were those who: 1) did not fly; 2) had symptoms before flying but flew anyhow; 3) and did not have symptoms before flying but developed symptoms during or after flight. Of the total DCS population, 13.9% had preflight symptoms while 5.6% developed symptoms during or after flight. Symptoms which occurred during or after flight were no more serious and their responses to recompression no less successful than symptoms in nonflying divers. There was a statistically significant association between divers who flew with pre-existing symptoms and Type II DCS, incomplete relief with one recompression, and residual symptoms after 3 months.

Effect of a single air dive on pulmonary diffusing capacity in professional divers.

The aim of this study was to determine whether venous gas embolism after a single air dive, evaluated using precordial Doppler monitoring, was associated with alterations in spirometry, lung volumes, arterial blood gases, or pulmonary diffusing capacity for carbon monoxide (DLCO). Postdive time course monitoring of pulmonary function was undertaken in 10 professional divers exposed to absolute air pressure of 5.5 bar for 25 min in a dry walk-in chamber. The US Navy decompression table was followed. Venous bubbles were detected by precordial Doppler monitoring. Two types of decompression were used: air and 100% O2 applied for 21 min during decompression stops. Spirometry, flow-volume, and body plethysmography parameters were unchanged after the dive with air decompression (AD) as well as with O2 decompression (OD). A significant reduction in arterial PO2, on average 20 Torr, was found after the dive with AD. DLCO was decreased in all divers 20, 40, 60, and 80 min after diving with AD (P < 0.001), whereas it was not significantly decreased after diving with OD. Maximal DLCO decrease of approximately 15% occurred 20 min postdive. In AD diving, maximum bubble grade for each individual vs. maximum DLCO reduction correlated significantly (r = 0.85, P = 0.002), as well as DLCO vs. arterial PO2 (r = 0.64, P = 0.017). In conclusion, a reduction in pulmonary diffusing capacity is observed in parallel with the appearance of venous bubbles detected by precordial Doppler. We suggest that bubbles cause pulmonary microembolization, triggering a complex sequence of events that remains to be resolved. Measuring DLCO complements Doppler bubble detection in postdiving assessment of pulmonary function.

Lung diffusing capacity in a hyperbaric environment: assessment by a rebreathing technique.

A rebreathing method was developed for measuring diffusing lung capacity for carbon monoxide (DLCO) in a hyperbaric environment. Twenty two professional naval divers with normal lung function were included in the study. Significant correlations were found between rebreathing and single breath measurements for DLCO (r = 0.94; p less than 0.001; standard error of the estimate (SEE) = 0.66), alveolar volume (VA) (r = 0.79; p less than 0.005; SEE = 0.51), and DLCO/VA (r = 0.83; p less than 0.001; SEE = 0.11). In 17 divers, rebreathing DLCO (DLCOrb) was also measured at 20 minutes pre-dive, during the first decompression stop of the dive to 45 m for 25 minutes, and at 10 minutes post-dive. Compressed air diving was performed in a dry walk-in chamber and the United States Navy decompression table was followed. The pressure induced decrease in the rate of CO binding to haemoglobin was adjusted to normobaric conditions using a theoretical approach. Also, the presence of venous bubbles post-dive was detected by precordial doppler monitoring. A biphasic change in DLCO was noted: initially, DLCO was increased during the dive (p less than 0.005); this was followed by a post-dive decrease; DLCO/VA changed in a similar manner, as VA was only slightly altered. Only a small post-dive precordial doppler bubble grade was found. In conclusion, rebreathing DLCO measurement is a useful respiratory function test in the hyperbaric environment. It appears that an increase in D(L)CO during the compressed air dive is related predominantly to increased pulmonary capillary blood volume caused by increased negativity of the pleural pressure, hyperoxic pulmonary vasodilatation, and cardiorespiratory centralisation of the blood. The decrease in D(L)CO post-dive was only partially related to the presence of the venous bubbles detectable by doppler.

Effect of hyperbaric oxygenation on maximal aerobic performance in a normobaric environment.

Eighteen female physical education students, randomly divided into three groups, inhaled 100% O2 for 60 minutes in a hyperbaric chamber. Pressure in the chamber amounted to 2.8 ATA. Three days before the hyperbaric oxygenation (HBO) all the students were subjected to a treadmill test. The first group was retested after 30 minutes, the second after 3 hours and the third 6 hours after the HBO. The first and the second groups of subjects achieved statistically significant maximal oxygen consumption after the HBO (14.4 and 10% respectively) and were capable of sustaining considerably higher exertion on treadmill (12.8%, namely 18.1%, both values were significant on the level of p less than 0.05). The ventilation efficiency parameters (VEO2 and R) did not differ with any of the three groups of subject during the exertion before and after the HBO, although after the HBO the exertion was considerably higher.

Suppression of rat tumor colonies in the lung by oxygen at high pressure is a local effect.

The effect of hyperbaric oxygen (HBO) on the growth of anaplastic carcinoma colonies in rat lungs after intravenous tumor cell injection was studied. From the first day after tumor cell injection, the rats were exposed to HBO for 16-21 days, 90 min per day. Oxygen at a pressure of 300 kPa (3.0 ATA) significantly decreased the number of lung tumor colonies and increased the survival of tumor-bearing rats, whereas the application of oxygen at a pressure of 100 kPa had no effect. An oxygen-nitrogen normoxic mixture balanced with nitrogen to 300 kPa (3.0 ATA) did not affect the number of colonies, suggesting that the effect was specific for oxygen and not for the increased pressure itself. A 6-day application of oxygen at a 300 kPa pressure suppressed the growth of lung tumor colonies when applied on days 1-6 and 7-12 after intravenous tumor cell injection, but had no effect when applied on days 13-18. In contrast to dramatic effects of HBO on the development of artificial lung metastases, the oxygen at the same 300 kPa pressure had no effect on the growth of tumor cells injected in the hind foot. Thus it appears that the suppression of lung tumor colonies by HBO was due to local oxygen effects in the lungs.