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Flying after diving: should recommendations be reviewed? In-flight echocardiographic study in bubble-prone and bubble-resistant divers 2015 DAN Europe Research Division, Contrada Padune 11, 64026 Roseto degli, Abruzzi (TE), Italy, Phone: +39(0)85-893-0333, Fax: +39-(0)85-893-0050, E-mail: dcialoni@daneurope.org.; DAN Europe Research Division, Roseto degli Abruzzi, Italy.; DAN Europe Research
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Journal Article
Periodical, Full
Diving and hyperbaric medicine
Periodical, Abbrev.
Diving.Hyperb.Med.
Pub Date Free Form
Mar
Volume
45
Issue
1
Start Page
10
Other Pages
15
Notes
JID: 101282742; OTO: NOTNLM; 2014/12/12 [received]; 2015/01/17 [accepted]; ppublish
Place of Publication
Australia
ISSN/ISBN
1833-3516; 1833-3516
Accession Number
PMID: 25964033
Language
eng
SubFile
Journal Article; Research Support, Non-U.S. Gov't; IM
DOI
Output Language
Unknown(0)
PMID
25964033
Abstract
INTRODUCTION: Inert gas accumulated after multiple recreational dives can generate tissue supersaturation and bubble formation when ambient pressure decreases. We hypothesized that this could happen even if divers respected the currently recommended 24-hour pre-flight surface interval (PFSI). METHODS: We performed transthoracic echocardiography (TTE) on a group of 56 healthy scuba divers (39 male, 17 female) as follows: first echo--during the outgoing flight, no recent dives; second echo--before boarding the return flight, after a multiday diving week in the tropics and a 24-hour PFSI; third echo--during the return flight at 30, 60 and 90 minutes after take-off. TTE was also done after every dive during the week's diving. Divers were divided into three groups according to their 'bubble-proneness': non-bubblers, occasional bubblers and consistent bubblers. RESULTS: During the diving, 23 subjects never developed bubbles, 17 only occasionally and 16 subjects produced bubbles every day and after every dive. Bubbles on the return flight were observed in eight of the 56 divers (all from the 'bubblers' group). Two subjects who had the highest bubble scores during the diving were advised not to make the last dive (increasing their PFSI to approximately 36 hours), and did not demonstrate bubbles on the return flight. CONCLUSIONS: Even though a 24-hour PFSI is recommended on the basis of clinical trials showing a low risk of decompression sickness (DCS), the presence of venous gas bubbles in-flight in eight of 56 divers leads us to suspect that in real-life situations DCS risk after such a PFSI is not zero.
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Authors
Cialoni,D., Pieri,M., Balestra,C., Marroni,A.
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URL
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Editors
Inner-ear decompression sickness: 'hubble-bubble' without brain trouble? 2015 Deptartment of Neurology, San Gerardo Hospital and University of Milano-Bicocca, Italy, E-mail: lucio.tremolizzo@unimib.it.; Emergency Medical Service, Ventotene Island, Italy.; Deptartment of Neurology, San Gerardo Hospital and University of Milano-Bicoc
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Journal Article
Periodical, Full
Diving and hyperbaric medicine
Periodical, Abbrev.
Diving.Hyperb.Med.
Pub Date Free Form
Jun
Volume
45
Issue
2
Start Page
135
Other Pages
136
Notes
JID: 101282742; OTO: NOTNLM; ppublish
Place of Publication
Australia
ISSN/ISBN
1833-3516; 1833-3516
Accession Number
PMID: 26165540
Language
eng
SubFile
Case Reports; Letter; IM
DOI
Output Language
Unknown(0)
PMID
26165540
Abstract
Inner-ear decompression sickness (DCS) is an incompletely understood and increasingly recognized condition in compressed-air divers. Previous reports show a high association of inner-ear DCS with persistent foramen ovale (PFO), suggesting that a moderate-to-severe right-to-left shunt might represent a major predisposing factor, and more properly de fi ning it as an event from arterial gas embolism (AGE). However, other conditions characterized by bubbles entering the arterial circulation, such as open-chamber cardiac surgery, do not produce inner-ear involvement, while sometimes damaging the brain extensively. Moreover, in other sites, such as the spinal cord, the prevailing mechanism for DCS is not AGE, but more likely local bubble formation with subsequent compression of venules and capillaries. Thus, AGE might be, more properly, a predisposing condition, neither suf fi cient, nor possibly even strictly necessary for inner-ear DCS. A 'two-hit hypothesis' has been proposed, implying a locally selective vulnerability of the inner ear to AGE. Modelled kinetics for gas removal are slower in the inner ear compared to the brain, leading to a supersaturated environment which allows bubbles to grow until they eventually obstruct the labyrinthine artery. Since this artery is relatively small, there is a low probability for a bubble to enter it; this might explain the disproportion between the high prevalence of PFO in the general population (25-30%) and the very low incidence of inner-ear DCS in compressed-air diving (approximately 0.005%). Furthermore, given that the labyrinthine artery usually originates either from the anterior inferior cerebellar artery, or directly from the basilar artery, shunting bubbles will more frequently swarm through the entire brain. In this case, however, the brain's much faster gas removal kinetics might allow for them to be reabsorbed without damaging brain tissue. In line with this scenario is the low probability (approx. 15%) of inner-ear DCS presenting with concomitant symptoms suggestive of brain involvement. Interestingly, PFO is a putative risk factor not only for DCS but also for ischaemic stroke, and it has been hypothesized that a predominantly silent ischaemic cerebral burden might represent a meaningful surrogate of end-organ damage in divers with PFO, with implications for stroke or cognitive decline. Here we report the case of a 44-year-old diving instructor (> 350 dives) who suffered from inner-ear DCS about 10 min after a routine dive (5 min/40 metres' fresh water (mfw), ascent 7.5 mfw.min(-)(1), stop 10 min/5 mfw), resulting in severe left cochlear/vestibular impairment (complete deafness and marked vertigo, only the latter slowly receding after a few hours). The patient was not recompressed. A few months later, transcranial Doppler ultrasonography demonstrated a moderate-to-severe shunt (> 30 bubbles), presumably due to a PFO (he refused confirmatory echocardiography), while a brain MRI (1.5 T) was reported as negative for both recent and remote lacunar infarcts (Figure 1). We believe this may be evidence that inner-ear DCS could occur while the brain is completely spared, not only clinically, but also at neuroimaging. This would support either of two hypotheses: (a) that the brain is indeed relatively protected from arterial bubbles that preferentially harm the inner ear where, however, they only rarely in fi ltrate, or (b) that direct bubble formation within the inner ear cannot be completely discarded, and that the elevated PFO-inner-ear DCS association might be, in this latter case, merely circumstantial. We favour the hypothesis that inner-ear DCS might be related to AGE in an anatomically vulnerable region. More precise data regarding the exact incidence of inner-ear involvement, isolating those subjects with moderate-to-severe shunt, should be obtained before exploring the risk-to-bene fi t ratio given by transcatheter occlusion of a PFO for prevention of inner-ear DCS; odds th
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Tremolizzo,L., Malpieri,M., Ferrarese,C., Appollonio,I.
Original/Translated Title
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Editors
Presence of dipalmitoylphosphatidylcholine from the lungs at the active hydrophobic spots in the vasculature where bubbles are formed on decompression 2016 Israel Naval Medical Institute rarieli@netvision.net.il.; Department of Oxidative Stress and Human Diseases, MIGAL - Galilee Research Institute and Tel Hai College, Kiryat Shmona.; Department of Oxidative Stress and Human Diseases, MIGAL - Galilee Researc
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Journal Article
Periodical, Full
Journal of applied physiology (Bethesda, Md.: 1985)
Periodical, Abbrev.
J.Appl.Physiol.(1985)
Pub Date Free Form
11-Aug
Volume
Issue
Start Page
jap.00649.2016
Other Pages
Notes
LR: 20160812; CI: Copyright (c) 2016; JID: 8502536; OTO: NOTNLM; 2016/08/10 [accepted]; 2016/07/19 [received]; aheadofprint; SO: J Appl Physiol (1985). 2016 Aug 11:jap.00649.2016. doi: 10.1152/japplphysiol.00649.2016.
Place of Publication
ISSN/ISBN
1522-1601; 0161-7567
Accession Number
PMID: 27516538
Language
ENG
SubFile
JOURNAL ARTICLE
DOI
10.1152/japplphysiol.00649.2016 [doi]
Output Language
Unknown(0)
PMID
27516538
Abstract
Most severe cases of decompression illness (DCI) are caused by vascular bubbles. We showed that there are active hydrophobic spots (AHS) on the luminal aspect of ovine blood vessels where bubbles are produced after decompression. It has been suggested that AHS may be composed of lung surfactant. Dipalmitoylphosphatidylcholine (DPPC) is the main component of lung surfactants. Blood samples and four blood vessels, the aorta, superior vena cava, pulmonary vein and pulmonary artery, were obtained from 11 slaughtered sheep. Following exposure to 1013 kPa for 20.4 h, we started photographing the blood vessels 15 min after the end of decompression for a period of 30 min, to determine AHS by observing bubble formation. Phospholipids were extracted from AHS and from control tissue and plasma for determination of DPPC. DPPC was found in all blood vessel samples and all samples of plasma. The concentration of DPPC in the plasma samples (n = 8) was 2.04+/-0.90 microg/ml. The amount of DPPC in the AHS which produced four or more bubbles (n = 16) was 1.59+/-0.92 microg. This was significantly higher than the value obtained for AHS producing less than four bubbles and for control samples (n = 19) (0.97+/-0.61 microg, P = 0.027). DPPC leaks from the lungs into the blood, settling on the luminal aspect of the vasculature to create AHS. Determining the constituents of the AHS might pave the way for their removal, resulting in a dramatic improvement in diver safety.
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Journal of Applied Physiology
Data Source
Authors
Arieli,R., Khatib,S., Vaya,J.
Original/Translated Title
URL
Date of Electronic
20160811
PMCID
Editors
Arterial gas bubbles after decompression in pigs with patent foramen ovale 1993 Section for Extreme Work Environment, Sintef Unimed, Trondheim, Norway.
Source Type
Print(0)
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Journal Article
Periodical, Full
Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc
Periodical, Abbrev.
Undersea Hyperb.Med.
Pub Date Free Form
Jun
Volume
20
Issue
2
Start Page
121
Other Pages
131
Notes
LR: 20071115; JID: 9312954; 0 (Gases); ppublish
Place of Publication
UNITED STATES
ISSN/ISBN
1066-2936; 1066-2936
Accession Number
PMID: 8329939
Language
eng
SubFile
Journal Article; Research Support, Non-U.S. Gov't; IM; S
DOI
Output Language
Unknown(0)
PMID
8329939
Abstract
With patent foramen ovale (PFO), thought to be a risk factor for some forms of DCS, venous bubbles may pass through the patent opening to become arterial bubbles. We exposed 14 anesthetized, spontaneously breathing pigs to air at 5 bar (500 kPa, absolute pressure) for 30 min and then rapidly decompressed at 2 bar/min to 1 bar. We measured intravascular pressures, blood gases, and, with transesophageal echocardiology, bubbles in the pulmonary artery and ascending aorta. Autopsy showed that six of the pigs had a PFO. Arterial bubbles occurred more frequently in the PFO group (in six out of six) than in the non-PFO group (in two out of eight, P < 0.01). When arterial bubbles were detected, the venous bubble count and the pulmonary artery pressure tended to be lower in pigs with PFO than in pigs without a PFO. We conclude that a PFO increases the risk of arterial bubbles after decompression.
Descriptors
Animals, Atmosphere Exposure Chambers, Decompression Sickness/blood/etiology/physiopathology, Embolism, Air/blood/etiology/physiopathology, Gases/blood, Heart Septal Defects, Atrial/blood/complications/physiopathology, Hemodynamics/physiology, Swine
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Data Source
Authors
Vik,A., Jenssen,B. M., Brubakk,A. O.
Original/Translated Title
URL
Date of Electronic
PMCID
Editors
Bubble formation and decompression sickness on direct ascent from shallow air saturation diving 1993 Maritime Self-Defense Force, Undersea Medical Center, Yokosuka, Japan.
Source Type
Print(0)
Ref Type
Journal Article
Periodical, Full
Aviation, Space, and Environmental Medicine
Periodical, Abbrev.
Aviat.Space Environ.Med.
Pub Date Free Form
Feb
Volume
64
Issue
2
Start Page
121
Other Pages
125
Notes
LR: 20041117; JID: 7501714; ppublish
Place of Publication
UNITED STATES
ISSN/ISBN
0095-6562; 0095-6562
Accession Number
PMID: 8431185
Language
eng
SubFile
Case Reports; Journal Article; IM; S
DOI
Output Language
Unknown(0)
PMID
8431185
Abstract
To find the minimum supersaturation pressure for detectable bubble formation and for contraction of decompression sickness (DCS), three shallow air saturation dives at the depth of 6 m, 7 m, and 8 m were performed. The ultrasonic M-mode method was used for detecting bubbles. The exposure period was 3 d for all dives. Ten subjects were compressed to both 6 m and 7 m, and nine subjects were compressed to 8 m. One bubble streak was shown in the 6-m dive group. A small number of bubbles were seen in four subjects in the 7-m dive. All subjects in the 8-m dive presented various amounts of bubbles. DCS was not observed in the 6-m and 7-m dives. On the other hand, in the 8-m dive, four subjects suffered from DCS and required recompression treatment. The minimum depth for detectable bubble formation was assessed at around 6 m and the direct ascent from saturation at 8 m seems to have a high risk of DCS.
Descriptors
Adult, Decompression Sickness, Diving, Embolism, Air/etiology/ultrasonography, Humans, Male, Middle Aged
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Data Source
Authors
Ikeda,T., Okamoto,Y., Hashimoto,A.
Original/Translated Title
URL
Date of Electronic
PMCID
Editors