Evolutionary genetics of pulmonary anatomical adaptations in deep-diving cetaceans.

BACKGROUND: Cetaceans, having experienced prolonged adaptation to aquatic environments, have undergone evolutionary changes in their respiratory systems. This process of evolution has resulted in the emergence of distinctive phenotypic traits, notably the abundance of elastic fibers and thickened alveolar walls in their lungs, which may facilitate alveolar collapse during diving. This structure helps selective exchange of oxygen and carbon dioxide, while minimizing nitrogen exchange, thereby reducing the risk of DCS. Nevertheless, the scientific inquiry into the mechanisms through which these unique phenotypic characteristics govern the diving behavior of marine mammals, including cetaceans, remains unresolved. RESULTS: This study entails an evolutionary analysis of 42 genes associated with pulmonary fibrosis across 45 mammalian species. Twenty-one genes in cetaceans exhibited accelerated evolution, featuring specific amino acid substitutions in 14 of them. Primarily linked to the development of the respiratory system and lung morphological construction, these genes play a crucial role. Moreover, among marine mammals, we identified eight genes undergoing positive selection, and the evolutionary rates of three genes significantly correlated with diving depth. Specifically, the SFTPC gene exhibited convergent amino acid substitutions. Through in vitro cellular experiments, we illustrated that convergent amino acid site mutations in SFTPC contribute positively to pulmonary fibrosis in marine mammals, and the presence of this phenotype can induce deep alveolar collapse during diving, thereby reducing the risk of DCS during diving. CONCLUSIONS: The study unveils pivotal genetic signals in cetaceans and other marine mammals, arising through evolution. These genetic signals may influence lung characteristics in marine mammals and have been linked to a reduced risk of developing DCS. Moreover, the research serves as a valuable reference for delving deeper into human diving physiology.

Real-time imaging of decompression gas bubble growth in the spinal cord of live rats.

PURPOSE: To observe the growth and resolution of decompression gas bubbles in the spinal cord of live rats in real time using MRI. METHODS: We constructed an MRI-compatible pressure chamber system to visualize gas bubble dynamics in deep tissues in real time. The system pressurizes and depressurizes rodents inside an MRI scanner and monitors their respiratory rate, heart rate, and body temperature while providing gaseous anesthesia under pressure during the experiments. RESULTS: We observed the formation of decompression gas bubbles in the spinal cord of rats after compression to 7.1 bar absolute and rapid decompression inside the MRI scanner while maintaining continuous gaseous anesthesia and vital monitoring. CONCLUSION: We have shown the direct observation of decompression gas bubble formation in real time by MRI in live, anesthetized rats.

Eccentric exercise before a 90 min exposure at 24,000 ft increases decompression strain depending on body region but not total muscle mass recruited.

Eccentric upper-body exercise performed 24 h prior to high-altitude decompression has previously been shown to aggravate venous gas emboli (VGE) load. Yet, it is unclear whether increasing the muscle mass recruited (i.e., upper vs. whole-body) during eccentric exercise would exacerbate the decompression strain. Accordingly, this study aimed to investigate whether the total muscle mass recruited during eccentric exercise influences the decompression strain. Eleven male participants were exposed to a simulated altitude of 24,000 ft for 90 min on three separate occasions. Twenty-four hours before each exposure, participants performed one of the following protocols: (i) eccentric whole-body exercise (ECCw; squats and arm-cycling exercise), (ii) eccentric upper-body exercise (ECCu; arm-cycling), or (iii) no exercise (control). Delayed onset muscle soreness (DOMS) and isometric strength were evaluated before and after each exercise intervention. VGE load was evaluated at rest and after knee- and arm-flex provocations using the 6-graded Eftedal-Brubakk scale. Knee extensor (-20 ± 14%, P = 0.001) but not elbow flexor (-12 ± 18%, P = 0.152) isometric strength was reduced 24 h after ECCw. ECCu reduced elbow flexor isometric strength at 24 h post-exercise (-18 ± 10%, P < 0.001). Elbow flexor DOMS was higher in the ECCu (median 6) compared with ECCw (5, P = 0.035). VGE scores were higher following arm-flex provocations in the ECCu (median (range), 3 (0-4)) compared with ECCw (2 (0-3), P = 0.039) and control (0 (0-2), P = 0.011), and in ECCw compared with control (P = 0.023). VGE were detected earlier in ECCu (13 ± 20 min) compared with control (60 ± 38 min, P = 0.021), while no differences were noted between ECCw (18 ± 30 min) and control or ECCu. Eccentric exercise increased the decompression strain compared with control. The VGE load varied depending on the body region but not the total muscle mass recruited. HIGHLIGHTS: What is the central question of this study? Does exercise-induced muscle damage (EIMD) resulting from eccentric exercise influence the presence of venous gas emboli (VGE) during a 90 min continuous exposure at 24,000 ft? What is the main finding and its importance? EIMD led to an earlier manifestation and greater VGE load compared with control. However, the decompression strain was dependent on the body region but not the total muscle mass recruited.

Decompression sickness of the inner ear and relationship with a patent oval foramen: a study of 61 cases.

OBJECTIVE: To discuss the link between inner ear decompression sickness and patent foramen ovale. MATERIALS AND METHODS: Monocentric and retrospective study on decompression sickness of the inner ear requiring hyperbaric chamber treatment, from 2014 to 2021. RESULTS: Sixty-one patients of inner ear decompression sickness were included in this study. Twenty-four patients had vestibular injuries, 28 cochlear injuries and 9 cochleo-vestibular injuries. Compression chamber treatment was given, using an oxygen-helium mixture with oxygen partial pressure (PIO2) limited to 2.8 atmosphere absolute (ATA). All vestibular accidents completely recovered without clinical sequelae. For cochlear accident only 10 out of 37 patients (27%) recovered completely. A right-left shunt (patent foramen oval or intra-pulmonary shunt) was found in 31.1% of patients with inner ear decompression sickness (p > 0.05). CONCLUSION: The presence of patent foramen oval in patients with inner ear decompression was not statistically significant in our study. Understanding of the pathophysiology of decompression illness and the physiology and anatomy of the labyrinth would suggest a mechanism of supersaturation with degassing in intra-labyrinthine liquids.

Decompression sickness followed by diabetic ketoacidosis and sepsis shock: an unusual case report.

Decompression sickness (DCS) is caused by abrupt changes in extracorporeal pressure with varying severity. Symptoms range from mild musculoskeletal pain to severe organ dysfunction and death, especially among patients with chronic underlying disease. Here, we report an unusual case of a 49-year-old man who experienced DCS after a dive to a depth of 38 meters. The patient's symptoms progressed, starting with mild physical discomfort that progressed to disturbance of consciousness on the second morning. During hospitalization, we identified that in addition to DCS, he had also developed diabetic ketoacidosis, septic shock, and rhabdomyolysis. After carefully balancing the benefits and risks, we decided to provide supportive treatment to sustain vital signs, including ventilation support, sugar-reducing therapy, fluid replacement, and anti-infection medications. We then administered delayed hyperbaric oxygen (HBO2) when his condition was stable. Ultimately, the patient recovered without any sequelae. This is the first case report of a diver suffering from DCS followed by diabetic ketoacidosis and septic shock. We have learned that when DCS and other critical illnesses are highly suspected, it is essential to assess the condition comprehensively and focus on the principal contradiction.

In-field use of I-VED electrical impedance sensor for assessing post-dive decompression stress in humans.

Purpose: Ultrasound imaging is commonly used in decompression research to assess venous gas emboli (VGE) post-dive, with higher loads associated with increased decompression sickness risk. This work examines, for the first time in humans, the performance of a novel electrical impedance spectroscopy technology (I-VED), on possible detection of post-dive bubbles presence and arterial endothelial dysfunction that may be used as markers of decompression stress. Methods: I-VED signals were recorded in scuba divers who performed standardized pool dives before and at set time points after their dives at 35-minute intervals for about two hours. Two distinct frequency components of the obtained signals, Low-Pass Frequency-LPF: 0-0.5 Hz and Band-Pass Frequency-BPF: 0.5-10 Hz, are extracted and respectively compared to VGE presence and known flow-mediated dilation trends for the same dive profile for endothelial dysfunction. Results: Subjects with VGE counts above the median for all subjects were found to have an elevated average LPF compared to subjects with lower VGE counts, although this was not statistically significant (p=0.06), as well as significantly decreased BPF standard deviation post-dive compared to pre-dive (p=0.008). Conclusions: I-VED was used for the first time in humans and operated to provide qualitative in-vivo electrical impedance measurements that may contribute to the assessment of decompression stress. Compared to ultrasound imaging, the proposed method is less expensive, not operator-dependent and compatible with continuous monitoring and application of multiple probes. This study provided preliminary insights; further calibration and validation are necessary to determine I-VED sensitivity and specificity.

[The otolaryngologist's role in evaluating diving fitness]. / Beurteilung einer Tauchtauglichkeit als HNO-Arzt.

Scuba diving and other modes of device-supported diving are popular activities that can be especially demanding and hazardous for people with preexisting physical conditions. Due to the high ambient pressure, the temperature differences, and potential unpredictable events, which have manifold effects on the organism, diving carries a high risk of life-threatening disease. A special risk is present if the body does not readily equalize air pressure changes. Therefore, prior to diving, all divers should undergo detailed education regarding the physical principles of the sport as well as specific physical examination. Consultation of an otolaryngologist is of exceptional relevance because many otorhinolaryngologic diseases can lead to (usually temporary) unfitness to dive. The role of the modern otorhinolaryngologist trained in diving medicine is to correctly advise the patient and restore fitness for diving via conservative or invasive methods.

The involvement of transient receptor potential channels in mast cell activation by microbubbles.

This study was to explore the activation of mast cells by microbubbles, with the focus on transient receptor potential (TRP) channels mediated degranulation and calcium influx. Bone marrow-derived mast cells (BMMCs) were primarily obtained from femurs in mice and induced differentiation for 4 weeks. After the purity identification, BMMCs were contacted by homogeneous microbubbles with the diameter of 1 mm for 1 h. ß-hexosaminidase and histamine levels in supernatants were assessed by enzyme-linked immunosorbent assay (ELISA) and the CD63 expression was tested by flow cytometry. The intracellular calcium binding with Fluo-4 AM dyes in BMMCs was observed under the fluorescence microscope and the mean fluorescence intensity was quantitatively measured by flow cytometry. ß-hexosaminidase release, histamine concentration, CD63 expression and calcium influx were significantly increased in BMMCs group upon microbubble stimulation compared to the control groups. After preconditioning with the available inhibitors and microbubble contact, only transient receptor potential vanilloid 1 (TRPV1) and TRPV4 inhibitors robustly suppressed the microbubble-induced degranulation. Likewise, the elevated fluorescence intensity of cytosolic calcium level was also significantly weaken. The results demonstrated microbubble stimulus effectively promoted BMMCs degranulation, which could be substantially restrained by inhibitors targeted for blocking TRPV1 or TRPV4 channel. The alternation of intracellular calcium level in BMMCs was consistent with the changes of degranulation capacity. It's suggested that the activation of BMMCs by microbubbles may involve specific TRP calcium dependent channels.

Eccentric exercise 24 h prior to hypobaric decompression increases decompression strain.

PURPOSE: Animal studies have shown that recent musculoskeletal injuries increase the risk of decompression sickness (DCS). However, to date no similar experimental study has been performed in humans. The aim was to investigate if exercise-induced muscle damage (EIMD)-as provoked by eccentric work and characterized by reduced strength and delayed-onset muscle soreness (DOMS)-leads to increased formation of venous gas emboli (VGE) during subsequent hypobaric exposure. METHODS: Each subject (n = 13) was on two occasions exposed to a simulated altitude of 24,000 ft for 90 min, whilst breathing oxygen. Twenty-four hours prior to one of the altitude exposures, each subject performed 15 min of eccentric arm-crank exercise. Markers of EIMD were reduction in isometric m. biceps brachii strength and DOMS as assessed on the Borg CR10 pain scale. The presence of VGE was measured in the right cardiac ventricle using ultrasound, with measurements performed at rest and after three leg kicks and three arm flexions. The degree of VGE was evaluated using the six-graded Eftedal-Brubakk scale and the Kisman integrated severity score (KISS). RESULTS: Eccentric exercise induced DOMS (median 6.5), reduced the biceps brachii strength (from 230 ± 62 N to 151 ± 8.8 N) and increased the mean KISS at 24,000 ft, both at rest (from 1.2 ± 2.3 to 6.9 ± 9.2, p = 0.01) and after arm flexions (from 3.8 ± 6.2 to 15.5 ± 17.3, p = 0.029). CONCLUSION: EIMD, induced by eccentric work, provokes release of VGE in response to acute decompression.

Decompression strain in parachute jumpmasters during simulated high-altitude missions: a special reference to preoxygenation strategies.

PURPOSE: Military parachute operations are often executed at high altitude, from an unpressurized aircraft compartment. Parachute jumpmasters (JM) are thus regularly exposed to 29,500 ft for 60 min. The aim was to investigate the decompression strain during a simulated JM mission at high altitude and to compare two strategies of preoxygenation, conducted either at sea-level or below 10,000 ft, during ascent to mission altitude. METHODS: Ten JM completed, on separate occasions, a 45-min preoxygenation either at sea-level (normobaric: N) or 8200ft (hypobaric: H), followed by exposure to 28,000 ft for 60 min, whilst laying supine and breathing 100% oxygen. At min 45 of the exposure to 28,000 ft, the JM performed 10 weighted squats. Decompression strain was determined from ultrasound assessment of venous gas emboli (VGE) during supine rest (5-min intervals), after three unloaded knee-bends (15-min intervals) and immediately following the weighted squats. The VGE were scored using a six-graded scale (0-5). RESULTS: In condition H, two JM experienced decompression sickness (DCS), whereas no DCS incidents were reported in condition N. The prevalence of VGE was higher in the H than the N condition, at rest [median(range), 3(0-4) vs 0(0-3); p = 0.017], after unloaded knee-bends [3(0-4) vs 0(0-3); p = 0.014] and after the 10 weighted squats [3(0-4) vs 0(0-3); p = 0.014]. VGE were detected earlier in the H (28 ± 20 min, p = 0.018) than the N condition (50 ± 19 min). CONCLUSIONS: A preoxygenation/altitude procedure commonly used by JM, with a 60-min exposure to 28,000 ft after pre-oxygenation for 45 min at 8200 ft is associated with high risk of DCS. The decompression strain can be reduced by preoxygenating at sea level.

A prospective observational study on the effect of emboli exposure on cerebral autoregulation in cardiac surgery requiring cardiopulmonary bypass.

OBJECTIVE: Cerebrovascular autoregulation impairment has been associated with stroke risk in cardiac surgery. We hypothesized that greater arterial emboli exposure in open-chamber surgery might promote dysautoreguation. METHODS: Forty patients underwent closed or open-chamber surgery. Transcranial Doppler detected emboli and measured bilateral middle cerebral artery flow velocities. Cerebral autoregulation was assessed by averaging the mean velocity index ("Mx," a continuous moving correlation between cerebral blood flow velocity and mean arterial pressure) over 30 min before and after aortic cross-clamp removal. RESULTS: Median (interquartile range) emboli counts were 775 (415, 1211) and 2664 (793, 3734) in the closed-chamber and open-chamber groups. Most appeared after the removal of the aortic cross-clamp (open-chamber 1631 (606, 2296)), (closed-chamber 229 (142, 384)), with emphasis on the right hemisphere (open-chamber: 826 (371, 1622)), (closed-chamber 181 (66, 276)). Linear mixed model analyses of mean velocity index change showed no significant overall effect of group (0.08, 95% CI: -0.04, 0.21; p = 0.19) or side (0.01, 95% CI: -0.03, 0.05; p = 0.74). There was an interaction between group and side (p = 0.001), manifesting as a greater increase in mean velocity index in the right hemisphere in the open than the closed group (mean difference: 0.15, 95% CI: 0.02, 0.27; p = 0.03). CONCLUSIONS: Overall, change in mean velocity index before and after cross-clamp removal did not differ between groups. However, most emboli entered the right cerebral hemisphere where this change was significantly greater in the open-chamber group, suggesting a possible association between embolic exposure and dysautoregulation.

Elevations of Extracellular Vesicles and Inflammatory Biomarkers in Closed Circuit SCUBA Divers.

Blood-borne extracellular vesicles and inflammatory mediators were evaluated in divers using a closed circuit rebreathing apparatus and custom-mixed gases to diminish some diving risks. "Deep" divers (n = 8) dove once to mean (±SD) 102.5 ± 1.2 m of sea water (msw) for 167.3 ± 11.5 min. "Shallow" divers (n = 6) dove 3 times on day 1, and then repetitively over 7 days to 16.4 ± 3.7 msw, for 49.9 ± 11.9 min. There were statistically significant elevations of microparticles (MPs) in deep divers (day 1) and shallow divers at day 7 that expressed proteins specific to microglia, neutrophils, platelets, and endothelial cells, as well as thrombospondin (TSP)-1 and filamentous (F-) actin. Intra-MP IL-1ß increased by 7.5-fold (p < 0.001) after day 1 and 41-fold (p = 0.003) at day 7. Intra-MP nitric oxide synthase-2 (NOS2) increased 17-fold (p < 0.001) after day 1 and 19-fold (p = 0.002) at day 7. Plasma gelsolin (pGSN) levels decreased by 73% (p < 0.001) in deep divers (day 1) and 37% in shallow divers by day 7. Plasma samples containing exosomes and other lipophilic particles increased from 186% to 490% among the divers but contained no IL-1ß or NOS2. We conclude that diving triggers inflammatory events, even when controlling for hyperoxia, and many are not proportional to the depth of diving.

A fully automated algorithm for heart rate detection in post-dive precordial Doppler ultrasound.

Background: Doppler ultrasound is used currently in decompression research for the evaluation of venous gas emboli (VGE). Estimation of heart rate from post-dive Doppler ultrasound recordings can provide a tool for the evaluation of physiological changes from decompression stress, as well as aid in the development of automated VGE detection algorithms that relate VGE presence to cardiac activity. Method: An algorithm based on short-term autocorrelation was developed in MATLAB to estimate the heart rate in post-dive precordial Doppler ultrasound. The algorithm was evaluated on 21 previously acquired and labeled precordial recordings spanning Kisman-Masurel (KM) codes of 111-444 (KM I-IV) with manually derived instantaneous heart rates. Results: A window size of at least two seconds was necessary for robust and accurate instantaneous heart rate estimation with a mean error of 1.56 ± 7.10 bpm. Larger window sizes improved the algorithm performance, at the cost of beat-to-beat heart rate estimates. We also found that our algorithm provides good results for low KM grade Doppler recordings with and without flexion, and high KM grades without flexion. High KM grades observed after movement produced the greatest mean absolute error of 6.12 ± 8.40 bpm. Conclusion: We have developed a fully automated algorithm for the estimation of heart rate in post-dive precordial Doppler ultrasound recordings.

Proposed Thalmann algorithm air diving decompression table for the Swedish Armed Forces.

The Swedish Armed Forces (SwAF) air dive tables are under revision. Currently, the air dive table from the U.S. Navy (USN) Diving Manual (DM) Rev. 6 is used with an msw-to-fsw conversion. Since 2017, the USN has been diving according to USN DM rev. 7, which incorporates updated air dive tables derived from the Thalmann Exponential Linear Decompression Algorithm (EL-DCM) with VVAL79 parameters. The SwAF decided to replicate and analyze the USN table development methodology before revising their current tables. The ambition was to potentially find a table that correlates with the desired risk of decompression sickness.  New compartmental parameters for the EL-DCM algorithm, called SWEN21B, were developed by applying maximum likelihood methods on 2,953 scientifically controlled direct ascent air dives with known outcomes of decompression sickness (DCS). The targeted probability of DCS for direct ascent air dives was ≤1% overall and ≤1‰ for neurological DCS (CNS-DCS). One hundred fifty-four wet validation dives were performed with air between 18 to 57 msw. Both direct ascent and decompression stop dives were conducted, resulting in incidences of two joint pain DCS (18 msw/59 minutes), one leg numbness CNS-DCS (51 msw/10 minutes with deco-stop), and nine marginal DCS cases, such as rashes and itching. A total of three DCS incidences, including one CNS-DCS, yield a predicted risk level (95% confidence interval) of 0.4-5.6% for DCS and 0.0-3.6% for CNS-DCS. Two out of three divers with DCS had patent foramen ovale. The SWEN21 table is recommended for the SwAF for air diving as it, after results from validation dives, suggests being within the desired risk levels for DCS and CNS-DCS.

Bubble rupture & viability of red blood cells under resonant acoustic standing waves.

Objective: The presentation of a novel prospective treatment for scenarios where bubble presence in the bloodstream poses a clinical risk. The method relies on generating resonant acoustic standing waves within a limb to non-invasively accelerate the dissolution of bubbles present in the bloodstream via bubble rupture. Additionally, a preliminary assessment of the effects of the resonant acoustic waves and bubble rupture events on red blood cell viability is provided. Methods: Two semicircular piezoelectric (PZT) transducers electrically connected to each other were assembled around a small-girth segment of a rear thigh removed from a swine specimen. When driven at the frequency of electric resonance, this swine thigh and PZT transducer arrangement generates resonant acoustic standing waves within the swine thigh. Consequently, mechanical resonance of the system was non-invasively established by monitoring the electric response of the PZT to the applied frequency. The resonant acoustic field generated was used for the detection and rupture of bubbles that travel through a simulated blood vessel installed across the swine thigh. Two sets of experiments were carried out using this methodology, one with the artificial blood vessel filled with saline solution and one with defibrinated sheep blood. For the latter case, a preliminary hematologic assessment was done with red blood cell counts. Conclusion: Resonant acoustic standing waves effectively rupture bubbles of 300µm to 900µm within a simplified swine thigh model. The average dissolved gas content was 44% due to resonant acoustic waves at powers above 20W. No significant effect on red blood cell counts was observed.

Hyperbaric treatment deviations for U.S. Navy divers: Spinal DCS.

Introduction: The United States Navy (USN) developed and refined standardized oxygen treatment tables for diving injuries, but USN tables may not address all situations of spinal decompression sickness (DCS). We describe a detailed recompression treatment regimen that deviated from standard USN protocol for an active-duty USN diver with a severe, delayed presentation of spinal cord DCS. Case Report: A USN diver surfaced from his second of three dives on a standard Navy 'no-Decompression' Air SCUBA dive (Max depth 101 fsw utilizing a Navy Dive Computer) and developed mid-thoracic back pain, intense nausea, paresthesias of bilateral feet, and penile erection. Either not recognizing the con- stellation of symptoms as DCS and after resolution of the aforementioned symptoms, he completed the third planned dive (essentially an in-water recompression). Several hours later, he developed paresthesias and numbness of bilateral feet and legs and bowel incontinence. He presented for hyperbaric treatment twenty hours after surfacing from the final dive and was diagnosed with severe spinal DCS. Based on the severity of clinical presentation and delay to treatment, the initial and follow-on treatments were modified from standard USN protocol. MRI of the spine four days after initial presentation demonstrated a 2.2 cm lesion at the T4 vertebral level extending caudally. Follow-up examinations over two years demonstrated almost complete return of motor and sensory function; however, the patient continued to suffer fecal incontinence and demonstrated an abnormal post-void residual urinary volume. An atypical presenting symptom, a discussion of MRI findings, and clinical correlations to the syndrome of spinal DCS are discussed throughout treatment and long-term recovery of the patient.

Varying Oxygen Partial Pressure Elicits Blood-Borne Microparticles Expressing Different Cell-Specific Proteins-Toward a Targeted Use of Oxygen?

Oxygen is a powerful trigger for cellular reactions, but there are few comparative investigations assessing the effects over a large range of partial pressures. We investigated a metabolic response to single exposures to either normobaric (10%, 15%, 30%, 100%) or hyperbaric (1.4 ATA, 2.5 ATA) oxygen. Forty-eight healthy subjects (32 males/16 females; age: 43.7 ± 13.4 years, height: 172.7 ± 10.07 cm; weight 68.4 ± 15.7 kg) were randomly assigned, and blood samples were taken before and 2 h after each exposure. Microparticles (MPs) expressing proteins specific to different cells were analyzed, including platelets (CD41), neutrophils (CD66b), endothelial cells (CD146), and microglia (TMEM). Phalloidin binding and thrombospondin-1 (TSP), which are related to neutrophil and platelet activation, respectively, were also analyzed. The responses were found to be different and sometimes opposite. Significant elevations were identified for MPs expressing CD41, CD66b, TMEM, and phalloidin binding in all conditions but for 1.4 ATA, which elicited significant decreases. Few changes were found for CD146 and TSP. Regarding OPB, further investigation is needed to fully understand the future applications of such findings.

Decompression sickness with incidental pulmonary cyst.

Decompression sickness (DCS) is a known complication of scuba diving. DCS occurs when bubbles are formed as pressure is reduced during and after ascent from a dive, following inert gas uptake during the dive. The bubbles cause inflammation and hypoxia. The definitive treatment for decompression sickness is hyperbaric oxygen therapy. We present a case of a healthy 16-year-old male who presented with decompression sickness and an incidental pulmonary cyst discovered by chest CT, likely congenital. The patient was successfully treated with U.S. Navy Treatment Table 6 (TT6) for his decompression sickness, but he continued to have chest pain, requiring hospitalization and consultation with pediatric pulmonology and cardiothoracic surgery from the cyst. Three years later he complained of chest pain with changes in altitude. Chest CT showed persistence of this cyst, and additional cysts. Case conference with pulmonologists and chest radiologist could not offer a definite etiology without lung biopsy, felt to not be indicated. We believe that the changes in pressure/volumes during the dives and TT6 exacerbated his pulmonary cyst.

Efficiency of a 24-hour on-call system for early recompression therapy for acute decompression sickness.

Background: Early recompression therapy is suggested for a better clinical outcome of decompression sickness (DCS) patients. This study analyzed the efficacy of our 24-hour on-call system for early recompression therapy. Methods: We conducted a single-center retrospective cohort study. They were classified into DCS Type I versus Type II, duty time versus non-duty time groups based on the time of emergency department (ED) admission, and hospitalization versus discharge groups according to clinical outcomes. Baseline characteristics, diving variables, and in-hospital course were analyzed. Results: This study investigated 341 acute DCS patients. A total of 81 and 260 patients had Type I and Type II DCS, respectively. While 198 patients accessed the center during duty time, 143 presented during non-duty time. Fifty patients were admitted, and 291 patients were discharged. Total median time from symptom onset to HBO2 therapy was 259 minutes: 240 minutes for the duty group and 292 minutes for the non-duty group (p=0.16); 251 minutes for the discharged group and 291 minutes for the hospitalized group (p<0.001). The median time from ED admission to HBO2 therapy was 65 minutes: 60 minutes for the duty group and 69 minutes for the non-duty group (p=0.23); 63.4 minutes for the discharged group and 92 minutes for the hospitalized group (p=0.05). Conclusion: The 24-hour on-call system was able to provide acute DCS patients with early recompression therapy even during non-duty time. However, in terms of the outcome of treatment of patients, quicker arrival at the hospital and swifter recompression therapy are needed.

Post-decompression bubble and inflammation interactions: a non-extensive dynamical system model.

Inert gas bubbles in tissues and in blood have been historically considered as the only triggering factors for DCS, but now many other factors are considered to affect the final outcome of a decompression profile for a certain individual. In this sense, inflammation seems to play a relevant role, not only due to the physical damage of tissues by the bubbles, but as a potentiator of the process as a whole. The present study aims to put forward a mathematical model of bubble formation associated with an inflammatory process related to decompression. The model comprises four state-variables (inert gas pressure, inert gas bubbles, proinflammatory and inflammatory factors) in a set of non-linear differential equations. The model is non-extensive: inert gas transitions between liquid and gaseous phases do not change the concentration of the dissolved gas. The relationship between bubbles and inflammation is given through parameters that form a positive feedback loop. The results of the model were compared with the experimental results of echocardiography from volunteers in two dive/decompression profiles; the model shows a very good agreement with the empirical data and previews different inflammatory outcomes for different experimental profiles. We suggest that slight changes in the parameters' values might turn the simulations from a non-inflammatory to an inflammatory profile for a given individual. Therefore, the present model might help address the problem of DCS on a particular basis.