Risk Of Decompression Illness Research Articles

The risk of decompression illness in breath-hold divers: a systematic review

Breath-hold (BH) diving has known risks, for example drowning, pulmonary oedema of immersion and barotrauma. There is also the risk of decompression illness (DCI) from decompression sickness (DCS) and/or arterial gas embolism (AGE). The first report on DCS in repetitive freediving was published in 1958 and from then there have been multiple case reports and a few studies but no prior systematic review or meta-analysis. We undertook a systematic literature review to identify articles available from PubMed and Google Scholar concerning breath-hold diving and DCI up to August 2021. The present study identified 17 articles (14 case reports, three experimental studies) covering 44 incidences of DCI following BH diving. This review found that the literature supports both DCS and AGE as potential mechanisms for DCI in BH divers; both should be considered a risk for this cohort of divers, just as for those breathing compressed gas while underwater.

Decompression Illness Incidence and Hypoxia Symptoms After Prebreathing in Hypobaric Hypoxia Training.

INTRODUCTION: Hypobaric hypoxia training utilizing the environmental chamber is often preceded by prebreathing of 100% oxygen with the goal of reducing decompression illness (DCI). We aimed to study the impact of prebreathing 100% oxygen for 30 min prior to hypobaria exposure to 7600 m (25,000 ft) on the incidence rate of DCI, as well as the impact of prebreathing on hypoxia symptoms felt during training.METHODS: Records of participants who underwent hypobaric hypoxia training in the Republic of Singapore Air Force (RSAF) from 2011 to 2014 (before introduction of prebreathing) were compared to those who underwent similar training from 2014 to 2017 (after introduction of prebreathing) to determine the incidences of DCI for both groups. Participants who underwent hypobaric hypoxia training from January 2017 to July 2017 completed a survey to assess the impact of prebreathing on the presentation and severity of hypoxia symptoms.RESULTS: Two DCI events were recorded in 1530 hypobaric chamber exposures without prebreathing while two DCI events were recorded in 1729 exposures with prebreathing. There was no significant difference in the incidence of DCI between the two groups. The survey findings showed no significant difference in the presentation and severity of hypoxia symptoms with 30 min of prebreathing.DISCUSSION: Incidence of DCI remains low during hypobaric chamber training, with no statistical difference with or without prebreathing. Possible reasons were the short duration of hypobaric exposure of 10 min during hypoxia training, and that 30 min of prebreathing was insufficient to further decrease or eliminate the risk of DCI in short duration hypobaric exposures.Cheok LJ, Goh BLY, Soh FW, Chuan BTB. Decompression illness incidence and hypoxia symptoms after prebreathing in hypobaric hypoxia training. Aerosp Med Hum Perform. 2021; 92(5):289293.

Nanobubbles Form at Active Hydrophobic Spots on the Luminal Aspect of Blood Vessels: Consequences for Decompression Illness in Diving and Possible Implications for Autoimmune Disease-An Overview.

Decompression illness (DCI) occurs following a reduction in ambient pressure. Decompression bubbles can expand and develop only from pre-existing gas micronuclei. The different hypotheses hitherto proposed regarding the nucleation and stabilization of gas micronuclei have never been validated. It is known that nanobubbles form spontaneously when a smooth hydrophobic surface is submerged in water containing dissolved gas. These nanobubbles may be the long sought-after gas micronuclei underlying decompression bubbles and DCI. We exposed hydrophobic and hydrophilic silicon wafers under water to hyperbaric pressure. After decompression, bubbles appeared on the hydrophobic but not the hydrophilic wafers. In a further series of experiments, we placed large ovine blood vessels in a cooled high pressure chamber at 1,000 kPa for about 20 h. Bubbles evolved at definite spots in all the types of blood vessels. These bubble-producing spots stained positive for lipids, and were henceforth termed “active hydrophobic spots” (AHS). The lung surfactant dipalmitoylphosphatidylcholine (DPPC), was found both in the plasma of the sheep and at the AHS. Bubbles detached from the blood vessel in pulsatile flow after reaching a mean diameter of ~1.0 mm. Bubble expansion was bi-phasic—a slow initiation phase which peaked 45 min after decompression, followed by fast diffusion-controlled growth. Many features of decompression from diving correlate with this finding of AHS on the blood vessels. (1) Variability between bubblers and non-bubblers. (2) An age-related effect and adaptation. (3) The increased risk of DCI on a second dive. (4) Symptoms of neurologic decompression sickness. (5) Preconditioning before a dive. (6) A bi-phasic mechanism of bubble expansion. (7) Increased bubble formation with depth. (8) Endothelial injury. (9) The presence of endothelial microparticles. Finally, constant contact between nanobubbles and plasma may result in distortion of proteins and their transformation into autoantigens.

Frequency of decompression illness among recent and extinct mammals and "reptiles": a review.

The frequency of decompression illness was high among the extinct marine "reptiles" and very low among the marine mammals. Signs of decompression illness are still found among turtles but whales and seals are unaffected. In humans, the risk of decompression illness is five times increased in individuals with Patent Foramen Ovale; this condition allows blood shunting from the venous circuit to the systemic circuit. This right-left shunt is characteristic of the "reptile" heart, and it is suggested that this could contribute to the high frequency of decompression illness in the extinct reptiles.

Decompression illness - critical review

Decompression illness is caused by intravascular or extravascular bubbles that are formed as a result of reduction in environmental pressure (decompression). The term covers both arterial gas embolism, in which alveolar gas or venous gas emboli (via cardiac shunts or via pulmonary vessels) are introduced into the arterial circulation, and decompression sickness, which is caused by in-situ bubble formation from dissolved inert gas. Both syndromes can occur in divers, compressed air workers, aviators, and astronauts, but arterial gas embolism also arises from iatrogenic causes unrelated to decompression. Risk of decompression illness is affected by immersion, exercise, and heat or cold. Manifestations range from itching and minor pain to neurological symptoms, cardiac collapse, and death. First-aid treatment is 1 0 0 % oxygen and definitive treatment is recompression to increased pressure, breathing 1 0 0 % oxygen. Adjunctive treatment, including fluid administration and prophylaxis against venous thromboembolism in paralysed patients, is also recommended Treatment is, in most cases, effective although residual deficits can remain in serious cases, even after several recompressions.

Hyperbaric Oxygen Therapy for Radionecrosis: Clear Advice From Confusing Data

TO THE EDITOR: The study by Annane et al violated an ethical principle by exposing the control group to the potentially serious risk of acute decompression illness; a risk not present in the treatment group. The trial involved the control group breathing a gas mixture of 9% oxygen and 91% nitrogen at treatment pressure (the placebo) to simulate breathing air at atmospheric pressure. This procedure requires mandatory decompression (controlled return to atmospheric pressure) to de-nitrogen the patients. This decompression was not a requirement for the oxygenbreathing (treatment) group. Decompression dives are not advised by some sports scuba diving organizations. Additionally, Annane et al, are mistaken in stating “a similar placebo has recently been used to evaluate HBO [hyperbaric oxygen therapy].” In the trial, they found that the control arm breathed a mixture of 60% nitrogen, 40% oxygen, negating the risk of decompression illness. Another issue requiring clarification is the number of patients who actually completed their prescribed treatment sessions. For example, the data show that at least 75% of the treatment group failed to receive the protocol minimum of 30 treatments. Furthermore, 26 of patients (48.1%) in stage A mandibular osteoradionecrosis at enrolment progressed to stage B, thus requiring them to complete a total of 40 sessions. No clear information is given about the compliance of these patients. Their Table 2 also indicated that very few sessions were stopped due to complications. Thus the question arises, why did at least 75% of patients not complete 30 treatments and what of the subgroup requiring 40? Additionally, it is unclear how in Table 2 there can be two patients with two sessions “discontinued due to complications,” but only one patient with two sessions in which complication arose. Other anomalies detract the reader from accepting the trial design and execution. For example, as with development, the evolution of osteoradionecrosis is variable. How was this variable accounted for in the small numbers involved in the triangular test? It would also be of interest to know how many of the 12 participating centers used hyperbaric oxygen before the trial and how many (if any) have continued with its use. As the accompanying editorial points out, this study is “under-powered.” Therefore, to conclude with an unequivocal statement based on a trial involving literally only a handful of compliant patients is surprising. This study does, however, highlight that further research is urgently needed before giving any definitive advice about treating this painful and debilitating condition.

Risk of decompression illness among 230 divers in relation to the presence and size of patent foramen ovale

Dear Sirs, Sandra Rea Torti et al., in the June issue of the Journal ,1 report on a group of divers, examined for patency of the foramen ovale (PFO), and claim to be able to calculate the relative risk for decompression illness (DCI) when a diver has a PFO. Where it is true that in large samples with a low occurrence of a disease in proportion to a risk factor, the Odds Ratio may approach the value of the Relative Risk, in this series that claim is unjustified.2 First of all, the authors undertook a retrospective …

Risk of decompression illness among 230 divers in relation to the presence and size of patent foramen ovale

Risk of decompression illness among 230 divers in relation to the presence and size of patent foramen ovale

Risk of decompression illness among 230 divers in relation to the presence and size of patent foramen ovale.

The risk of developing decompression illness (DCI) in divers with a patent foramen ovale (PFO) has not been directly determined so far; neither has it been assessed in relation to the PFO's size. In 230 scuba divers (age 39+/-8 years), contrast trans-oesophageal echocardiography (TEE) was performed for the detection and size grading (0-3) of PFO. Prior to TEE, the study individuals answered a detailed questionnaire about their health status and about their diving habits and accidents. For inclusion into the study, > or =200 dives and strict adherence to decompression tables were required. Sixty-three divers (27%) had a PFO. Overall, the absolute risk of suffering a DCI event was 2.5 per 10(4) dives. There were 18 divers (29%) with, and 10 divers (6%) without, PFO who had experienced > or =1 major DCI events P=0.016. In the group with PFO, the incidence per 10(4) dives of a major DCI, a DCI lasting longer than 24 h and of being treated in a decompression chamber amounted to 5.1 (median 0, interquartile range [IQR] 0-10.0), 1.9 (median 0, IQR 0-4.0) and 3.6 (median 0, IQR 0-9.8), respectively and was 4.8-12.9-fold higher than in the group without PFO (P<0.001). The risk of suffering a major DCI, of a DCI lasting longer than 24 h and of being treated by recompression increased with rising PFO size. The presence of a PFO is related to a low absolute risk of suffering five major DCI events per 10(4) dives, the odds of which is five times as high as in divers without PFO. The risk of suffering a major DCI parallels PFO size.

Right-to-left shunt and risk of decompression illness with cochleovestibular and cerebral symptoms in divers: case control study in 101 consecutive dive accidents.

We investigated the role of right-to-left shunt with standardized transcranial Doppler ultrasonography in a large population of divers referred for symptoms of decompression illness. Case series compared with a control group. Military teaching hospital, hyperbaric unit. Patients were 101 consecutive divers with clinical evidence of decompression illness and a control group of 101 healthy divers. Specification of the type of decompression illness involved and detection/evaluation of right-to-left shunt by standardized transcranial Doppler. The degree of right-to-left shunt was defined as major if the number of high-intensity transient signals in the middle cerebral artery was >20. We evaluated the odds ratios by logistic regression analysis with vs. without right-to-left shunt for subjects with cochleovestibular symptoms, cerebral decompression illness, spinal decompression illness, and Caisson sickness. Of the 101 divers presenting with decompression illness, transcranial Doppler detected a right-to-left shunt in 59 (58.4%), whereas control subjects demonstrated a right-to-left shunt in 25 cases (24.8%; odds ratio, 4.3; 95% confidence interval, 2.3-7.8; p=.09). When a right-to-left shunt was detected, the right-to-left shunt was major in 12 of 25 patients in the control group and in 49 of 59 patients in the decompression illness group (odds ratio, 8.7; 95% confidence interval, 4.2-18.0; p<.001). Within the decompression illness group, the proportion of major right-to-left shunt was 24 of 34 (odds ratio, 29.7; 95% confidence interval, 10.0-87.2; p<.0001) in the cochleovestibular subgroup, 13 of 21 (odds ratio, 24.1, 95% confidence interval, 6.8-86.0, p< 0.0001) in the cerebral decompression illness subgroup, ten of 31 (odds ratio, 3.9; 95% confidence interval, 1.5-10.3; p<.01) in the spinal decompression illness subgroup, and two of two (odds ratio, 1.1; 95% confidence interval, 0.2-5.7; p=.9) in the subgroup of divers with Caisson sickness. Based on our results, we conclude that major right-to-left shunt was associated with an increased incidence of cochleovestibular and cerebral decompression illness, suggesting paradoxical embolism as a potential mechanism.

The Indigenous Fisherman Divers of Thailand: Diving Practices

Diving practices of a group of indigenous people living on Thailand’s west coast were investigated. Village chiefs were first interviewed using a questionnaire. Three hundred and forty-two active divers were then interviewed by health care workers using a second questionnaire. Field observation was used to further develop information and confirm diving practices. Divers in 6 villages, whose basic means of making a living is from diving for marine products such as fish and shellfish, have diving patterns that put them at substantial risk of decompression illness. Breathing air from a primitive compressor through approximately 100 m of air hose, these divers have long bottom times coupled with short surface intervals. Forty-six point two percent of the divers indicated that they would not make a stop during ascent from a long deep dive (40 m for 30 min). When comparing their previous day of diving to the U.S. Navy Standard Air Decompression Table (U.S. Navy, 1993), 72.1% exceeded the no-decompression limits set by the tables. Diving patterns point to a need for more in-depth research into the diving patterns of this indigenous group. Future research should include the use of dive logging devices to record depths and times. There is also a need to provide divers with information and training to reinforce positive practices and strengthen knowledge of the risks associated with their current diving practices.