An explicitly multi-component arterial gas embolus dissolves much more slowly than its one-component approximation.

We worked out the growth and dissolution rates of an arterial gas embolism (AGE), to illustrate the evolution over time of its size and composition, and the time required for its total dissolution. We did this for a variety of breathing gases including air, pure oxygen, Nitrox and Heliox (each over a range of oxygen mole fractions), in order to assess how the breathing gas influenced the evolution of the AGE. The calculations were done by numerically integrating the underlying rate equations for explicitly multi-component AGEs, that contained a minimum of three (water, carbon dioxide and oxygen) and a maximum of five components (water, carbon dioxide, oxygen, nitrogen and helium). The rate equations were straight-forward extensions of those for a one-component gas bubble. They were derived by using the Young-Laplace equation and Dalton's law for the pressure in the AGE, the Laplace equation for the dissolved solute concentration gradients in solution, Henry's law for gas solubilities, and Fick's law for diffusion rates across the AGE/arterial blood interface. We found that the 1-component approximation, under which the contents of the AGE are approximated by its dominant component, greatly overestimates the dissolution rate and underestimates the total dissolution time of an AGE. This is because the 1-component approximation manifestly precludes equilibration between the AGE and arterial blood of the inspired volatile solutes (O2, N2, He) in arterial blood. Our calculations uncovered an important practical result, namely that the administration of Heliox, as an adjunct to recompression therapy for treating a suspected N2-rich AGE must be done with care. While Helium is useful for preventing nitrogen narcosis which can arise in aggressive recompression therapy wherein the N2 partial pressure can be quite high (e.g.∼5 atm), it also temporarily expands the AGE, beyond the expansion arising from the use of Oxygen-rich Nitrox. For less aggressive recompression therapy wherein nitrogen narcosis is not a significant concern, Oxygen-rich Nitrox is to be preferred, both because it does not temporarily expand the AGE as much as Heliox, and because it is much cheaper and more conservation-minded.

Hyperbaric Oxygen Therapy Emergencies.

Emergent indications for HBO2 are not only for some of the most serious conditions, but also may be the only modality to directly target the patient's pathophysiology. They are to begin emergently or urgently, but may be limited by either the instability of the patient's condition or transfer logistics. Often these emergent treatments involve several treatments in the first 24 hours for best outcomes. If one considers the effects of HBO2 upon the body while breathing 100% oxygen at pressure many benefits become evident. This article will concisely review hyperbaric oxygen's emergent indications.

Nitrogen Washout and Venous Gas Emboli During Sustained vs. Discontinuous High-Altitude Exposures.

INTRODUCTION: The frequency of long-duration, high-altitude missions with fighter aircraft is increasing, which may increase the incidence of decompression sickness (DCS). The aim of the present study was to compare decompression stress during simulated sustained high-altitude flying vs. high-altitude flying interrupted by periods of moderate or marked cabin pressure increase.METHODS: The level of venous gas emboli (VGE) was assessed from cardiac ultrasound images using the 5-degree Eftedal-Brubakk scale. Nitrogen washout/uptake was measured using a closed-circuit rebreather. Eight men were investigated in three conditions: one 80-min continuous exposure to a simulated cabin altitude of A) 24,000 ft, or four 20-min exposures to 24,000 ft interspersed by three 20-min intervals at B) 20,000 ft or C) 900 ft.RESULTS: A and B induced marked and persistent VGE, with peak bubble scores of [median (range)]: A: 2.5 (1-3); B: 3.5 (2-4). Peak VGE score was less in C [1.0 (1-2), P < 0.01]. Condition A exhibited an initially high and exponentially decaying rate of nitrogen washout. In C the washout rate was similar in each period at 24,000 ft, and the nitrogen uptake rate was similar during each 900-ft exposure. B exhibited nitrogen washout during each period at 24,000 ft and the initial period at 20,000 ft, but on average no washout or uptake during the last period at 20,000 ft.DISCUSSION: Intermittent reductions of cabin altitude from 24,000 to 20,000 ft do not appear to alleviate the DCS risk, presumably because the pressure increase is not sufficient to eliminate VGE. The nitrogen washout/uptake rate did not reflect DCS risk in the present exposures.Ånell R, Grönkvist M, Eiken O, Gennser M. Nitrogen washout and venous gas emboli during sustained vs. discontinuous high-altitude exposures. Aerosp Med Hum Perform. 2019; 90(6):524-530.

A novel device for air removal from vascular access line: a bench study.

Efficient air removal from a vascular access line is a key step to prevent air embolism. Existing devices, especially for rapid infusers, are far from optimum. In this study, we developed a novel device, vascular access line air removal device (VALARD), and compared its efficiency of air removal and pause time of forward bulk flow with a commonly used device, the Belmont pump. Part I experiment, saline was infused at a forward bulk flow rate of 250, 500, and 750 mL/min. Meanwhile, air was introduced into the infusion line at a rate of 5, 10, and 15 mL/min for each bulk flow rate. Air bubbles > 10 µL downstream from either the VALARD or the Belmont pump and the fraction of pause time of the forward bulk flow were determined. Part II experiment, 120 mL of air was rapidly introduced into the VALARD at a bulk flow rate of about 500 mL/min. Air bubbles > 10 µL downstream from the VALARD, fraction of pause time of the forward bulk flow, and the transit time of the 120 mL of air at the working chamber were recorded. The VALARD: no air bubbles > 10 µL were detected during any tested combination of air injection and bulk flow rates without pause of forward flow. The Belmont pump: air bubbles > 10 µL were detected in 60% of the tests with pause of the forward flow. The VALARD eliminates air efficiently without pause of the forward bulk flow. Further clinical trials are needed to compare the VALARD with other devices and to assess its efficiency, safety, and user friendliness.

Thromboelastographic assessment of the impact of mexiletine on coagulation abnormalities induced by air or normal saline intravenous injections in conscious rats.

BACKGROUND: Thromboelastography (TEG) in venous air embolism (VAE) has been poorly studied. We induced coagulation abnormalities by VAE in a rat model, assessed by TEG with and without mexiletine, a lidocaine analogue local anesthetic. METHODS: Twenty-three Sprague Dawley rats instrumented under isoflurane anesthesia and allowed to recover five days prior to the experiments were randomized into three experimental groups: 1) VAE (n = 6); 2) VAE and mexiletine (n = 9); and 3) normal saline (NS) alone (control group, n = 8). Blood samples were collected at baseline, one hour (h) and 24 h in all groups and analyzed by TEG to record the R, K, angle α and MA parameters. RESULTS: In Group 1, VAE decreased significantly R at 1 h (31%), K at 1 h (59%) and 24 h (34%); α increased significantly at 1 h (30%) and 24 h (22%). While R returned to baseline values within 24 h, K, MA and α did not. In group-2 (Mexiletine + VAE), K and R decreased at 1 h (48% and 29%, respectively) and at 24 h the changes were non-significant. Angle α increased at 1 h (28%) and remained increased for 24 h (25%). In group 3 (NS), only R was temporarily affected. MA increased significantly at 24 h only in the VAE alone group. CONCLUSION: As expected, VAE produced a consistent and significant hypercoagulable response diagnosed/confirmed by TEG. Mexiletine prevented the MA elevation seen with VAE and corrected R and K time at 24 h, whereas angle α remained unchanged. Mexiletine seemed to attenuate the hypercoagulability associated with VAE in this experiment. These results may have potential clinical applications and deserve further investigation.

Venous gas emboli are involved in post-dive macro, but not microvascular dysfunction.

PURPOSE: Previous studies have shown vascular dysfunction of main conductance arteries and microvessels after diving. We aim to evaluate the impact of bubble formation on vascular function and haemostasis. To achieve this, we used a vibration preconditioning to influence bubble levels without changing any other parameters linked to the dive. METHODS: Twentty-six divers were randomly assigned to one of three groups: (1) the "vibrations-dive" group (VD; n = 9) was exposed to a whole-body vibration session 30 min prior the dive; (2) the "diving" group (D; n = 9) served as a control for the effect of the diving protocol; (3) The "vibration" protocol (V; n = 8) allowed us to assess the effect of vibrations without diving. Macro- and microvascular function was assessed for each subject before and after the dive, subsequently. Bubble grades were monitored with Doppler according to the Spencer grading system. Blood was taken before and after the protocol to assess any change of platelets or endothelial function. RESULTS: Bubble formation was lower in the VD than the diving group. The other measured parameters remained unchanged after the "vibration" protocol alone. Diving alone induced macrovascular dysfunction, and increased PMP and thrombin generation. Those parameters were no longer changed in the VD group. Conversely, a microvascular dysfunction persists despite a significant decrease of circulating bubbles. CONCLUSIONS: Finally, the results of this study suggest that macro- but not microvascular impairment results at least partly from bubbles, possibly related to platelet activation and generation of pro-coagulant microparticles.

Embolia aérea cerebral masiva tras colangiopancreatografía retrógrada endoscópica. Presentación de un caso y revisión de la bibliografía / Massive cerebral air embolism following endoscopic retrograde cholangiopancreatography. A case report and review of the literature

Introducción. La embolia aérea cerebral tras procesos endoscópicos es una complicación infrecuente, pero que puede tener consecuencias catastróficas. Caso clínico. Varón de 85 años, diagnosticado de colangiocarcinoma distal con criterios de irresecabilidad, al cual se coloca una prótesis biliar de drenaje. Se realiza una colangiopancreatografía retrógrada endoscópica para el cambio de prótesis. Tras el procedimiento, el paciente sufre un deterioro de las constantes vitales y del nivel de consciencia, y requiere intubación orotraqueal. En la tomografía axial computarizada craneal se evidencia una embolia aérea masiva con focos de isquemia hiperaguda en ambos hemisferios. El paciente fallece posteriormente. Conclusiones. El embolismo aéreo cerebral tras una colangiopancreatografía retrógrada endoscópica es infrecuente, pero potencialmente letal. La manipulación de la pared biliointestinal en las exploraciones endoscópicas podría originar comunicaciones entre la luz y el sistema venoso. Esto, unido a la alta presión de insuflación para la realización de la prueba, condicionaría el paso de aire al sistema venoso portal y, de ahí, al sistema circulatorio. En el sistema nervioso central, las burbujas de aire provocarían una obstrucción vascular, con la consiguiente isquemia y necrosis del tejido. Es fundamental un diagnóstico precoz y una terapia de soporte vital. Su rápido manejo puede contribuir a un mejor pronóstico, que en principio es sombrío (AU)

Introduction. Cerebral air embolism following endoscopic processes is an infrequent complication, but can have catastrophic consequences. Case report. An 85-year-old male diagnosed with distal cholangiocarcinoma with criteria for unresectability who was submitted to placement of a biliary drainage prosthesis. Endoscopic retrograde cholangiopancreatography was performed to change the prosthesis. After the procedure, the patient’s vital signs and level of consciousness underwent a decline, and orotracheal intubation was required. A computerised axial tomography scan of the head showed evidence of a massive air embolism with focal points of hyperacute ischaemia in both hemispheres. The patient later died. Conclusions. Cerebral air embolism following endoscopic retrograde cholangiopancreatography is infrequent, but potentially lethal. Manipulation of the bilio-intestinal wall in endoscopic examinations could give rise to communications between the lumen and the venous system. This, together with the high insufflation pressure used to conduct this test, would condition the passage of air to the portal venous system, and from there to the circulatory system. In the central nervous system, air bubbles would lead to a vascular obstruction, with the subsequent ischaemia and necrosis of tissues. An early diagnosis and life support therapy are essential. Its timely management can contribute to a better prognosis which, at least initially, is gloomy (AU)

Endothelial dysfunction correlates with decompression bubbles in rats.

Previous studies have documented that decompression led to endothelial dysfunction with controversial results. This study aimed to clarify the relationship between endothelial dysfunction, bubble formation and decompression rate. Rats were subjected to simulated air dives with one of four decompression rates: one slow and three rapid. Bubble formation was detected ultrasonically following decompression for two hours, before measurement of endothelial related indices. Bubbles were found in only rapid-decompressed rats and the amount correlated with decompression rate with significant variability. Serum levels of ET-1, 6-keto-PGF1α, ICAM-1, VCAM-1 and MDA, lung Wet/Dry weight ratio and histological score increased, serum NO decreased following rapid decompression. Endothelial-dependent vasodilatation to Ach was reduced in pulmonary artery rings among rapid-decompressed rats. Near all the above changes correlated significantly with bubble amounts. The results suggest that bubbles may be the causative agent of decompression-induced endothelial damage and bubble amount is of clinical significance in assessing decompression stress. Furthermore, serum levels of ET-1 and MDA may serve as sensitive biomarkers with the capacity to indicate endothelial dysfunction and decompression stress following dives.

Should Air Bubble Detectors Be Used to Quantify Microbubble Activity during Cardiopulmonary Bypass?

Air bubble detectors (ABDs) are utilized during cardiopulmonary bypass (CPB) to protect against massive air embolism. Stockert (Munich, Germany) ABD quantify microbubbles >300 µm; however, their reliability has not been reported. The aim of this study was to assess the reliability of the microbubble data from the ABD with the SIII and S5 heart-lung machines. Microbubble counts from the ABD with the SIII (SIII ABD) and S5 (S5 ABD) were measured simultaneously with the emboli detection and classification (EDAC) quantifier in 12 CPB procedures using two EDAC detectors and two ABDs in series in the arterial line. Reliability was assessed by the Spearman correlation co-efficient (r) between measurements for each detector type, and between each ABD and EDAC detector for counts >300 µm. No correlation was found between the SIII ABD (r = .008, p = .793). A weak negative correlation was found with the S5 ABD (r = -.16, p < .001). A strong correlation was found between the EDAC detectors (SIII; r = .958, p < .001), (S5; r = .908, p < .001). With counts >300 µm, the SIII ABDs showed a correlation of small-medium effect size between EDAC detectors and ABD1 (r = .286, p < .001 [EDAC1], r = .347, p < .001 [EDAC2]). There was no correlation found between ABD2 and either EDAC detector (r = .003, p = .925 (EDAC1), r = .003, p = .929 [EDAC2]). A correlation between EDAC and the S5 ABD, was not able to be determined due to the low bubble count detected by the EDAC >300 µm. Both SIII ABD and S5 ABD were found to be unreliable for quantification of microbubble activity during CPB in comparison with the EDAC. These results highlight the importance of ensuring that data included in the CPB report is accurate and clinically relevant, and suggests that microbubble counts from devices such as the SIII ABD and S5 ABD should not be reported.

Relationships between plasma lipids, proteins, surface tension and post-dive bubbles.

Decompression sickness (DCS) in divers is caused by bubbles of inert gas. When DCS occurs, most bubbles can be found in the venous circulation: venous gas emboli (VGE). Bubbles are thought to be stabilized by low molecular weight surfactant reducing the plasma-air surface tension (γ). Proteins may play a role as well. We studied the interrelations between these substances, γ and VGE, measured before and after a dry dive simulation. VGE of 63 dive simulations (21-msw/40-minute profile) of 52 divers was examined 40, 80, 120 and 160 minutes after surfacing (precordial Doppler method) and albumin, total protein, triglycerides, total cholesterol and free fatty acids were determined pre- and post-exposure. To manipulate blood plasma composition, half of the subjects obtained a fat-rich breakfast, while the other half got a fat-poor breakfast pre-dive. Eleven subjects obtained both. VGE scores measured with the precordial Doppler method were transformed to the logarithm of Kisman Integrated Severity Scores. With statistical analysis, including (partial) correlations, it could not be established whether γ as well as VGE scores are related to albumin, total protein or total cholesterol. With triglycerides and fatty acids correlations were also lacking, despite the fact that these compounds varied substantially. The same holds true for the paired differences between the two exposures of the 11 subjects. Moreover, no correlation between surface tension and VGE could be shown. From these findings and some theoretical considerations it seems likely that proteins lower surface tension rather than lipids. Since the findings are not in concordance with the classical surfactant hypothesis, reconsideration seems necessary.

High intensity cycling before SCUBA diving reduces post-decompression microparticle production and neutrophil activation.

BACKGROUND: Venous gas emboli (VGE) have traditionally served as a marker for decompression stress after SCUBA diving and a reduction in bubble loads is a target for precondition procedures. However, VGE can be observed in large quantities with no negative clinical consequences. The effect of exercise before diving on VGE has been evaluated with mixed results. Microparticle (MP) counts and sub-type expression serve as indicators of vascular inflammation and DCS in mice. The goal of the present study is to evaluate the effect of anaerobic cycling (AC) on VGE and MP following SCUBA diving. METHODS: Ten male divers performed two dives to 18 m for 41 min, one dive (AC) was preceded by a repeated-Wingate cycling protocol; a control dive (CON) was completed without exercise. VGE were analyzed at 15, 40, 80, and 120 min post-diving. Blood for MP analysis was collected before exercise (AC only), before diving, 15 and 120 min after surfacing. RESULTS: VGE were significantly lower 15 min post-diving in the AC group, with no difference in the remaining measurements. MPs were elevated by exercise and diving, however, post-diving elevations were attenuated in the AC dive. Some markers of neutrophil elevation (CD18, CD41) were increased in the CON compared to the AC dive. CONCLUSIONS: The repeated-Wingate protocol resulted in an attenuation of MP counts and sub-types that have been related to vascular injury and DCS-like symptoms in mice. Further studies are needed to determine if MPs represent a risk factor or marker for DCS in humans.

Can the oxygenator screen filter reduce gaseous microemboli?

Gaseous microemboli (GME) define small bubbles as < 200 microm in size. GME are reported to increase morbidity after cardiopulmonary bypass (CPB) and cardiac surgery. To prevent intrusion of GME into the systemic circulation during CPB, arterial line filtration is generally recommended. New trends in oxygenator design promote location of arterial filtration as an integral part of the oxygenator housing. The present experimental study aimed to evaluate the GME removal properties of an integrated arterial screen filter in a standard microporous oxygenator. The GME properties of Terumo Capiox FX25 with an integrated arterial screen filter was assessed in an experimental setup and compared with Capiox RX25, in which no arterial screen filter is present. A blood analog prime solution was recirculated using a roller pump at 4 and 6 L per minute flow rate, respectively, through a customized CPB circuit comprising oxygenator, reservoir, and connecting tubing. A controlled volume of air was introduced into the circuit. The GME activity was measured and computed using a Gampt BCC200 ultrasonic device placing one probe at the venous inlet and one other at the arterial outlet of the oxygenator. Transmembrane delta values of GME activity were used to calculate the removal efficacy based on counts and volume of GME. Use of screen filtration reduced the GME volume by 99.1% +/- .1% compared with 98.0% +/- .1% for controls at 4 L/min flow rate (p < .001). At 6 L/min, the reduction was 97.9% +/- .1% compared with 97.0% +/- .1% (p < .001). In contrast, the reduction of GME counts was less effective after screen filtration compared with controls: 89.6 +/- .6% versus 91.4 +/- .4% at 4 L/min and 55.6% +/- 1.6% versus 76.0% +/- 1.4% at 6 L/min, respectively (p < .001). The tested oxygenator with incorporated arterial screen filter reduced GME activity based on the calculated volume at the same time as counts of GME increased.

Microbubbles are detected prior to larger bubbles following decompression.

Using dual-frequency ultrasound (DFU), microbubbles (<10 µm diameter) have been detected in tissue following decompression. It is not known if these microbubbles are the precursors for B-mode ultrasound-detectable venous gas emboli (bmdVGE). The purpose of this study was to determine if microbubbles could be detected intravascularly postdecompression and to investigate the temporal relationship between microbubbles and larger bmdVGE. Anesthetized swine (n = 15) were exposed to 4.0-4.5 ATA for 2 h, followed by decompression to 0.98 ATA. Microbubble presence and VGE grade were measured using DFU and B-mode ultrasound, respectively, before and for 1 h postdecompression, approximately every 4-5 min. Microbubbles appeared in the bloodstream postdecompression, both in the presence and absence of bmdVGE. In swine without bmdVGE, microbubbles remained elevated for the entire 60-min postdecompression period. In swine with bmdVGE, microbubble signals were detected initially but then returned to baseline. Microbubbles were not detected with the sham dive. Mean bmdVGE grade increased over the length of the postdecompression data collection period. Comparison of the two response curves revealed significant differences at 5 and 10 min postdecompression, indicating that microbubbles preceded bmdVGE. These findings indicate that decompression-induced microbubbles can 1) be detected intravascularly at multiple sites, 2) appear in the presence and absence of bmdVGE, and 3) occur before bmdVGE. This supports the hypothesis that microbubbles precede larger VGE bubbles. Microbubble presence may be an early marker of decompression stress. Since DFU is a low-power ultrasonic method, it may be useful for operational diving applications.

Excessive negative venous line pressures and increased arterial air bubble counts during miniaturized cardiopulmonary bypass: an experimental study comparing miniaturized with conventional perfusion systems.

OBJECTIVES: Miniaturized cardiopulmonary bypass (MCPB) is increasingly used in cardiac surgery, because it can lower clinically significant complications such as systemic inflammatory response, haemolysis and high transfusion requirements. A limitation of MCPB is the risk of excessive negative pressure in the venous line during volume depletion, probably leading to gaseous microembolism. METHODS: In an experimental study with 24 pigs, we compared conventional open cardiopulmonary bypass (CCPB group, n = 11) with MCPB (n = 13). The same pump and identical tubing materials were used in both groups. Primary endpoints were pressure values in the venous line and the right atrium as well as the amount of air bubbles >500 µm. Secondary endpoints were biochemical parameters of systemic inflammatory response, ischaemia, haemodilution and haemolysis. RESULTS: Nearly 20% of venous pressure values were below -150 mmHg and approximately 10% of the right atrial pressure values were below -100 mmHg in the MCPB group, during the experiment. No such low values were observed in the CCPB group. In addition, the number of large arterial air bubbles was higher in the MCPB group compared with the CCPB group (mean ± standard deviation [SD]: 13 444 ± 5709 vs 0.9 ± 0.6, respectively; P < 0.001). Bubble volume was also significantly larger during MCPB compared with CCPB (mean ± SD: 1522 ± 654 vs 4.1 ± 2.5 µl, respectively; P < 0.001). Blood levels of interleukin-6, free haemoglobin and creatine kinase were significantly higher in the CCPB group compared with the MCPB group. CONCLUSIONS: Despite the benefits of MCPB regarding systemic inflammatory response and haemolysis, this technique is associated with excessive negative venous line pressures and a significant increase in the number and volume of arterial air bubbles compared with CCPB. Mini-perfusion systems and the management of MCPB require further refinements to avoid such adverse effects.

Body fat does not affect venous bubble formation after air dives of moderate severity: theory and experiment.

For over a century, studies on body fat (BF) in decompression sickness and venous gas embolism of divers have been inconsistent. A major problem is that age, BF, and maximal oxygen consumption (Vo2max) show high multicollinearity. Using the Bühlmann model with eight parallel compartments, preceded by a blood compartment in series, nitrogen tensions and loads were calculated with a 40 min/3.1 bar (absolute) profile. Compared with Haldanian models, the new model showed a substantial delay in N2 uptake and (especially) release. One hour after surfacing, an increase of 14-28% in BF resulted in a whole body increase of the N2 load of 51%, but in only 15% in the blood compartment. This would result in an increase in the bubble grade of only 0.01 Kisman-Masurel (KM) units at the scale near KM = I-. This outcome was tested indirectly by a dry dive simulation (air breathing) with 53 male divers with a small range in age and Vo2max to suppress multicollinearity. BF was determined with the four-skinfold method. Precordial Doppler bubble grades determined at 40, 80, 120, and 160 min after surfacing were used to calculate the Kisman Integrated Severity Score and were also transformed to the logarithm of the number of bubbles/cm(2) (logB). The highest of the four scores yielded logB = -1.78, equivalent to KM = I-. All statistical outcomes of partial correlations with BF were nonsignificant. These results support the model outcomes. Although this and our previous study suggest that BF does not influence venous gas embolism (Schellart NAM, van Rees Vellinga TP, van Dijk FH, Sterk W. Aviat Space Environ Med 83: 951-957, 2012), more studies with different profiles under various conditions are needed to establish whether BF remains (together with age and Vo2max) a basic physical characteristic or will become less important for the medical examination and for risk assessment.

The sitting position during neurosurgical procedures does not influence serum biomarkers of pulmonary parenchymal injury.

BACKGROUND: The sitting position during neurosurgical operations predisposes to air penetration through veins and the movement of the air through the pulmonary circulation. Contact of an air bubble with the endothelium can lead to acute lung injury. The presence of specific pulmonary proteins in the plasma such as surfactant protein D (SP-D) and Clara cell protein (CC16) is a biomarker of damaging processes at the air-blood barrier. The aim of our study was to examine the hypothesis that the level of investigated pulmonary biomarkers in plasma is higher in patients operated on in the sitting position. METHODS: The study included patients undergoing planned neurosurgical operations, who were divided into two groups: the sitting group (40 patients, operated on in the sitting position) and the supine group (24 patients, operated in the supine position). After the operation blood samples were drawn, centrifuged, frozen and stored until analyses were conducted. The determination of the SP-D and CC16 levels was performed using an ELISA test. Air embolism (VAE) was defined as a sudden drop in etCO2 of more than 2 mmHg and the presence of air bubbles in the aspirated blood from the central cannula. In all patients, the number of hospitalization days in the postoperative period was calculated. RESULTS: There were no differences in the average levels of SP-D between the groups (the mean in the sitting group was 95.56 ng/mL and the mean in the supine group was 101.21 ng/mL). The average levels of CC16 were similar in both groups as well (6.56 ng/mL in the sitting group and 6.79 ng/mL in the supine group). There was a statistically significant positive correlation between SP-D and CC16 values in both groups. VAE was diagnosed clinically in 12.5% of cases in the sitting group without a significant increase in SP-D and CC16 levels. On average, patients in both groups were discharged from the hospital within 9 days of surgery. CONCLUSION: The sitting position and intraoperative VAE during neurosurgical procedures do not affect the concentration of plasma biomarkers of pulmonary parenchymal injury such as SP-D and CC16.

Venous gas embolism after an open-water air dive and identical repetitive dive.

Decompression tables indicate that a repetitive dive to the same depth as a first dive should be shortened to obtain the same probability of occurrence of decompression sickness (pDCS). Repetition protocols are based on small numbers, a reason for re-examination. Since venous gas embolism (VGE) and pDCS are related, one would expect a higher bubble grade (BG) of VGE after the repetitive dive without reducing bottom time. BGs were determined in 28 divers after a first and an identical repetitive air dive of 40 minutes to 20 meters of sea water. Doppler BG scores were transformed to log number of bubbles/cm2 (logB) to allow numerical analysis. With a previously published model (Model2), pDCS was calculated for the first dive and for both dives together. From pDCS, theoretical logBs were estimated with a pDCS-to-logB model constructed from literature data. However, pDCS the second dive was provided using conditional probability. This was achieved in Model2 and indirectly via tissue saturations. The combination of both models shows a significant increase of logB after the second dive, whereas the measurements showed an unexpected lower logB. These differences between measurements and model expectations are significant (p-values < 0.01). A reason for this discrepancy is uncertain. The most likely speculation would be that the divers, who were relatively old, did not perform physical activity for some days before the first dive. Our data suggest that, wisely, the first dive after a period of no exercise should be performed conservatively, particularly for older divers.

Determinants of arterial gas embolism after scuba diving.

Scuba diving is associated with breathing gas at increased pressure, which often leads to tissue gas supersaturation during ascent and the formation of venous gas emboli (VGE). VGE crossover to systemic arteries (arterialization), mostly through the patent foramen ovale, has been implicated in various diving-related pathologies. Since recent research has shown that arterializations frequently occur in the absence of cardiac septal defects, our aim was to investigate the mechanisms responsible for these events. Divers who tested negative for patent foramen ovale were subjected to laboratory testing where agitated saline contrast bubbles were injected in the cubital vein at rest and exercise. The individual propensity for transpulmonary bubble passage was evaluated echocardiographically. The same subjects performed a standard air dive followed by an echosonographic assessment of VGE generation (graded on a scale of 0-5) and distribution. Twenty-three of thirty-four subjects allowed the transpulmonary passage of saline contrast bubbles in the laboratory at rest or after a mild/moderate exercise, and nine of them arterialized after a field dive. All subjects with postdive arterialization had bubble loads reaching or exceeding grade 4B in the right heart. In individuals without transpulmonary passage of saline contrast bubbles, injected either at rest or after an exercise bout, no postdive arterialization was detected. Therefore, postdive VGE arterialization occurs in subjects that meet two criteria: 1) transpulmonary shunting of contrast bubbles at rest or at mild/moderate exercise and 2) VGE generation after a dive reaches the threshold grade. These findings may represent a novel concept in approach to diving, where diving routines will be tailored individually.

Bubbles in live-stranded dolphins.

Bubbles in supersaturated tissues and blood occur in beaked whales stranded near sonar exercises, and post-mortem in dolphins bycaught at depth and then hauled to the surface. To evaluate live dolphins for bubbles, liver, kidneys, eyes and blubber-muscle interface of live-stranded and capture-release dolphins were scanned with B-mode ultrasound. Gas was identified in kidneys of 21 of 22 live-stranded dolphins and in the hepatic portal vasculature of 2 of 22. Nine then died or were euthanized and bubble presence corroborated by computer tomography and necropsy, 13 were released of which all but two did not re-strand. Bubbles were not detected in 20 live wild dolphins examined during health assessments in shallow water. Off-gassing of supersaturated blood and tissues was the most probable origin for the gas bubbles. In contrast to marine mammals repeatedly diving in the wild, stranded animals are unable to recompress by diving, and thus may retain bubbles. Since the majority of beached dolphins released did not re-strand it also suggests that minor bubble formation is tolerated and will not lead to clinically significant decompression sickness.