Feet Of Seawater Research Articles

Pulmonary Barotrauma in a BUD/S Candidate Following Shallow Dives Using the MK 25 Rebreather.

Pulmonary barotrauma of ascent is a well-recognized risk of compressed air diving in the civilian and military diving communities. Chest imaging is a beneficial adjunct to clinical evaluation in screening select individuals for fitness to dive, evaluating dive-related injuries, and safely returning individuals to diving duty. We present a case of a 26-year-old male U.S. Navy Ensign and Basic Underwater Demolition/SEAL (BUD/S) candidate who experienced pulmonary barotrauma following two shallow dives to a maximum depth of 18 feet of seawater using the MK-25 100% oxygen rebreather. A chest radiograph showed a left upper lobe peripheral wedge-shaped opacity abutting the pleural surface. A subsequent computerized tomography (CT) scan of the chest showed multifocal areas of peripheral pulmonary hemorrhage associated with small pneumatoceles. Two months after the diving injury, chest CT showed resolution of the pulmonary hemorrhage and pneumatoceles. Diving-related pulmonary barotrauma occurs most often secondary to breath-holding on ascent by inexperienced divers and is one of the most common diving injuries seen in BUD/S candidates. The risk of pulmonary barotrauma may be decreased through adequate training and thorough medical screening to include assessing for symptoms of infection before every dive. In cases of acute pulmonary barotrauma, chest radiographs may be used to screen for thoracic injury. Chest CT with inspiratory and expiratory sequences should be used to screen dive candidates on a case-by-case basis and to evaluate lung injury and predisposing pulmonary conditions following pulmonary barotrauma.

A DIVER WITH SWIMMING-INDUCED PULMONARY EDEMA AND CARDIAC ARREST

TOPIC: Occupational and Environmental Lung Diseases TYPE: Medical Student/Resident Case Reports INTRODUCTION: Swimming-induced pulmonary edema (SIPE) is classically considered to be a self-resolving, non-fatal condition that occurs in high exertion surface swimmers and divers. We report an unusual case of a scuba diver who had both SIPE and presumed cardiac arrest. CASE PRESENTATION: A 71-year old man with atrial fibrillation on apixaban, diabetes mellitus, and hypertension developed shortness of breath during a scuba dive at 50 feet of seawater. The maximum dive depth was 70 feet with an average water temperature of 67° Fahrenheit. He ascended per protocol. After being pulled onto the boat, the patient syncopized. Chest compressions and rescue breaths were initiated, and he regained consciousness 2-3 minutes later. Upon EMS arrival, the patient had oxygen saturation by pulse oximetry in the mid-70s. He was placed on 15 L/min of supplemental oxygen and transported to the hospital by helicopter. EKG and telemetry showed atrial fibrillation with a normal rate. Chest radiograph showed pulmonary edema, and CTA chest showed pulmonary edema with no pulmonary embolism. Transthoracic echocardiogram showed an ejection fraction of 55-60%, mild valvular disease, and no evidence of hypertrophy or shunting. Coronary angiogram showed mild non-obstructive coronary artery disease. The patient's hypoxia resolved within 24 hours of presentation, with resolution of the pulmonary edema on repeat chest radiograph. DISCUSSION: Swimming-induced pulmonary edema is primarily thought to be self-resolving and non-fatal. However, this case prompts the question of an association between SIPE and cardiac arrest that has not been described to our knowledge. The patient was presumed to have cardiac arrest, as opposed to non-cardiogenic syncope, given continued loss of consciousness during chest compressions. Coronary angiogram was pursued because the arrest was indistinguishable between sudden cardiac arrest (SCA) and provoked cardiac arrest, for example from hypoxia. SIPE is hypothesized to be a hydrostatic pulmonary edema that occurs due to elevated pulmonary artery pressures from increased peripheral vascular resistance and central redistribution of blood flow. Meanwhile, SCA is typically due to coronary disease, structural disease, or congenital arrhythmias. The absence of these pathologies in this patient suggest that SIPE may have played a distinct role in his SCA. Water immersion has been proposed to cause SCA through "autonomic conflict," whereby simultaneous sympathetic activation from exertion and parasympathetic activation from immersion increases likelihood of arrhythmia. However, the precise impact of SIPE on cardiac activity is not clear. CONCLUSIONS: Swimming induced pulmonary edema may have contributed to this patient's cardiac arrest. The possibility for life-threatening secondary complications of SIPE such as cardiac arrest warrants further investigation. REFERENCE #1: Spencer S, Dickinson J, Forbes L. Occurrence, Risk Factors, Prognosis and Prevention of Swimming-Induced Pulmonary Oedema: a Systematic Review [Internet]. Sport. Med. - Open. 2018 [cited 2021 Apr 28];4(1):43. REFERENCE #2: Moon RE, Martina SD, Peacher DF, et al. Swimming-induced pulmonary edema - Pathophysiology and Risk Reduction with Sildanefil. Circulation [Internet] 2016 [cited 2021 Apr 28];133(10):988–996. REFERENCE #3: Shattock MJ, Tipton MJ. 'Autonomic conflict': a different way to die during cold water immersion? J Physiol [Internet] 2012 [cited 2021 Apr 28];590(14):3219–3230. DISCLOSURES: No relevant relationships by Christopher Androski, source=Web Response Advisory Committee Member relationship with Actelion Please note: $5001 - $20000 by Richard Channick, source=Web Response, value=Consulting fee Consultant relationship with Actelion Please note: $5001 - $20000 by Richard Channick, source=Web Response, value=Consulting fee Advisory Committee Member relationship with Arena Please note: $5001 - $20000 by Richard Channick, source=Web Response, value=Consulting fee Advisory Committee Member relationship with Bayer Please note: $5001 - $20000 by Richard Channick, source=Web Response, value=Consulting fee Advisory Committee Member relationship with United Therapeutics Please note: $5001 - $20000 by Richard Channick, source=Web Response, value=Consulting fee No relevant relationships by Estebes Hernandez, source=Web Response No relevant relationships by Laura Santoso, source=Web Response No relevant relationships by Michael Tripp, source=Web Response

Decrease in dysbaric osteonecrosis severity as a result of 45-minute oxygen pre-breathe

Sudden decompression can result in bubble formation as the result of nitrogen gas (N2) dissolved in tissue during disabled submarine escape (DISSUB). This may cause dysbaric osteonecrosis (DON), a condition in long bones where bubbles in fatty marrow result in ischemia and necrosis. Previous research has shown that oxygen (O2) pre-breathe of two hours resulted in a reduction of DON; however, effects of shorter O2 pre-breathe remain uncertain. This study’s aim was to understand the effect of shorter lengths of O2 pre-breathe. Eight adult Suffolk ewes (89.5± 11.5 kg) were exposed to 33 feet of seawater (fsw) for 24 hours. They were placed randomly into four groups and exposed to either 45, 30 or 15 minutes of O2 (91-88%) pre-breathe; the controls received none. They were then rapidly decompressed. Alizarin complexone was later injected intravenously to visualize the extent of DON in the right and left long bones (radii, tibiae, femur and humeri). The 30- and 15-minute pre-breathe groups saw the greatest deposition. There was significant decrease of variance in the 45-minute group when compared with all other treatments, suggesting that 45 minutes of O2 pre-breathe is required to effectively increase confidence in the reduction of DON. Similar confidence was not reflected in the 30-minute and 15-minute groups: 45 minutes of pre-breathe was the minimum amount needed to effectively prevent against DON in DISSUB escape at 33 fsw. However, future research is needed to determine how to calculate effective dosages of O2 pre-breathe to prevent DON in any given scenario.

The effect of the perfluorocarbon emulsion OxycyteTM in an ovine model of severe decompression illness

Background: The treatment of decompression sickness (DCS) with hyperbaric oxygen (HBO2) serves to decrease intravascular bubble size, increase oxygen (O2) delivery to tissue and enhance the elimination of inert gas. Emulsified perfluorocarbons (PFC) combined with breathing O2 have been shown to have similar effects animal models. We studied an ovine model of severe DCS treated with the intravenous PFC OxycyteTM while breathing O2 compared to saline control also breathing O2. Methods: Juvenile male sheep (N=67; weight 24.4+/2.10kg) were compressed to 257 feet of sea water (fsw) in our multiple large-animal chamber where they remained under pressure for 31 minutes. Animals then were decompressed to surface pressure and randomized to receive either Oxycyte at 5mL/kg intravenously (IV) or 5mL/kg saline IV (both receiving 100% O2) 10 minutes after reaching surface pressure. Mortality was recorded at two hours, four hours, and 24 hours after receiving the study drug. Surviving animals underwent perfusion fixation and harvesting of the spinal cord at 24 hours. Spinal cord sections were assessed for volume of lesion area and compared. Results: There was no significant difference in survival at two hours (p=0.2737), four hours (p=0.2101), or 24 hours (p=0.3171). Paralysis at 24 hours was not significantly different. However, spinal cord lesion area was significantly smaller in the Oxycyte group as compared to the saline group, with median spinal cord lesion areas 0.65% vs. 0.94% (p=0.0107). Conclusions: In this ovine model of severe DCS the intravenous PFC Oxycyte did not reduce mortality but did ameliorate spinal cord injury when used after the onset of DCS.

CURIOUS CASE OF CAISSON DISEASE

SESSION TITLE: Medical Student/Resident Critical Care SESSION TYPE: Med Student/Res Case Report PRESENTED ON: October 18-21, 2020 INTRODUCTION: Decompression sickness is caused by rapid changes in breath air pressure and increased amounts of oxygen and nitrogen in different body tissues. As stated by Henry’s law, at a constant temperature the amount of gas dissolved is proportional to its partial pressure above the liquid. As the diver rapidly ascends, the air pressure substantially decreases creating air bubbles that can obstruct different blood vessels creating a wide variety of complications, including ischemia. With more than 9.5 million licensed divers, only 1,000 approximate cases of decompression sickness are reported per year, making it a rare diagnosis. CASE PRESENTATION: A 33 years-old male scuba diver was brought to the ED by ambulance after being found unconscious on the beach shore. Medical history consistent with MDD and cocaine dependence. While en route to the ED, developed neck pain, loss of muscle strength with preserved consciousness. Symptoms developed after five consecutives dives at 115 feet of sea water (fsw) without safety stops nor surface intervals. Spinal MRI was performed with findings consistent with acute isquemia at C6-T2 level. At this point the diagnosis of severe Caisson’s disease was made. Physical exam consisted of severe sensory neurologic impairment at level of T4-T5 dermatome accompanied by motor deficit in the lower extremities and left upper extremity motor deficit at level C8-T1. Initial laboratories showed increased coagulation factors and serum pH of 7.2. Immediately after diagnosis Hyperbaric Oxygen Therapy (HBO) was initiated. During his first session the patient developed respiratory distress and required endotracheal intubation. Follow up spinal MRI showed significant improvement of edema, however, patient’s neurological deficit persisted despite receiving corticosteroids and five HBO sessions. At this point the decision to continue HBO was made. By day 10 in the hospital the patient’s respiratory symptoms improved significantly and MV was discontinued. The patient completed a total of 20 sessions and regained complete movement and sensation in his body. He was discharged for inpatient rehabilitation where he completed therapy. DISCUSSION: This case illustrates the potential complications of decompression sickness and the importance of a prompt identification and rapid treatment to diminish the neurological sequelae and irreversible damage. Identifying precipitant factors that could further aggravate the ischemic symptoms are essential to decide whether the patient will benefit from an extended treatment. The decision to lengthen therapy with hyperbaric oxygen was conclusively beneficial despite delayed neurological improvement. Ultimately minimizing the tissue damage and increasing the odds of motor and sensory function recovery. CONCLUSIONS: Prolonged hyperbaric oxygen therapy could be beneficial in some patients. However, decisions should be made case by case. Reference #1: Hallenbeck, J. M., A. A. Bove, and D. H. Elliott. "Mechanisms underlying spinal cord damage in decompression sickness." Neurology 25.4 (1975): 308-308. Reference #2: Bühlmann, Albert A. Decompression—Decompression Sickness. Springer Science & Business Media, 2013. Reference #3: Weathersby, P. K., L. D. Homer, and E. T. Flynn. "On the likelihood of decompression sickness." Journal of Applied Physiology 57.3 (1984): 815-825. DISCLOSURES: No relevant relationships by Felix Aponte Santos, source=Web Response No relevant relationships by Rosa Marrero-Fernandez, source=Web Response No relevant relationships by Nikita Rabelo-Pagán, source=Web Response No relevant relationships by Nicole Rassi, source=Web Response No relevant relationships by Jean Rodriguez/Agramonte, source=Web Response

Decrease in Dysbaric Osteonecrosis Lesions as a Result of 45‐minute Oxygen Pre‐breathe

IntroductionNitrogen (N2) dissolved in long bone fatty marrow can lead to bubble formation in tissue when exposed to sudden decompression. During a disabled submarine escape (DISSUB) hastened decompression is often necessary, and formation of bubbles is likely. If recompression is not administered in a timely manner, bubbles may lead to ischemia and necrosis of marrow and bone, a condition called Dysbaric Osteonecrosis (DON). Oxygen (O2) pre‐breathe has been proposed as a way to reduce N2 in tissue, thus decreasing risk of DON. Previous research has shown that O2 pre‐breathe of 2‐hours resulted in a reduction in DON; however, effects of shorter O2 pre‐breathe are uncertain. This study’s aim is to understand the effect of shorter durations of O2 pre‐breathe on DON formation.MethodEight adult Suffolk ewes (89.5 ± 11.5 kg) were exposed to 33 feet of seawater (fsw) for 24 hours. Animals, separated at random into four groups (n=8) and exposed to either 45, 30, or 15 minutes of O2 (91–88%) pre‐breathe and 21% (controls), were rapidly decompressed. Four weeks after exposure and two weeks prior to euthanasia, Alizarin Complexone was injected intravenously to visualize areas of DON. Right and left long bones (radii, tibiae, femora, and humeri) were analyzed to determine the extent of Alizarin Complexone deposition. Percent deposition in the proximal, middle and distal thirds, as well as over the entire bone was calculated using areas of deposition and total bone to determine for extent of DON. Variance between the groups was found using an unpaired t‐test and Welch’s correction.ResultsA decrease in variance of DON occurrence was seen in the radius when comparing the 45‐minute (min) group to the 30‐min, 15‐min and the controls (p < 0.0001). The humerus also showed a similar decrease in variance when comparing groups (p < 0.05). Both the femur and tibia saw decreases in variance when comparing 45‐min group to the 30‐min and 15‐min group, (p < 0.0005) however no reduction was seen between the 45‐min group and the controls. The radius and tibia saw the highest rates of lesions. The radius mean depositions were 0.05 ± 0.07 in the 45‐min group, 4.8 ± 5.0 in the 30‐min group, 13.2 ± 14.8 in the 15‐min group and 6.4 ± 12.4 for the controls. The tibia mean depositions were 0.13 ± 0.18 in the 45‐min group, 4.8 ± 6.0 in the 30‐min group, 6.8 ± 11.2 in the 15‐min group and 0.6 ± 0.4 for the controls.DiscussionThe 30‐min, 15‐min and controls showed significant amounts of variability, which we hypothesize is due to differences in body composition. Similarly in humans, DON appears sporadically in those exposed to rapid decompression. The decrease of variance in the 45‐min group suggests that 45 minutes of O2 pre‐breathe is required to effectively increase confidence in the reduction of DON. Similar confidence was not reflected in the 30‐min and 15‐min groups. During DISSUB, speed of evacuation is vital for survival, our data suggests a minimum of 45 minutes of pre‐breathe is needed to confidently reduce the risk of developing DON. However, this duration may vary based on depth, time, body mass and bone composition. Future research is needed to understand the relationship between these variables in order to effectively calculate the sufficient O2 pre‐breathe required for an individual.Support or Funding InformationSupported by NAVSEA N00024‐17‐C‐4318

Safety of a continuous glucose monitoring device during hyperbaric exposure

Hyperbaric oxygen therapy has been demonstrated to lower blood glucose levels in patients with diabetes. Continuous glucose monitoring (CGM) allows glucose monitoring in real time. Battery-operated CGM transmitters have yet to be formally tested and given safety approval for use in a hyperbaric environment. We evaluated and tested commercially available Dexcom® G6 CGM transmitters under hyperbaric conditions. Each transmitter contains a 3V, 130-mAh (0.39 Wh) lithium manganese dioxide battery (IEC CR1632) and circuit board that are fully encapsulated in epoxy. Each transmitter is pressurized to 90 pounds per square inch (psi) in an autoclave at 40°C for up to 72 hours during manufacturing to ensure that all enclosed air spaces are eliminated from the epoxy. We compared the CGM components against section 14.2.9.3.17.5 of the 2018 National Fire Protection Association 99 (NFPA 99) Health Care Facilities Code requirements. Six CGM transmitters attached to estimated glucose value generators (EGVGs) underwent 11 pressurization cycles to 45 feet of seawater (fsw). All transmitters were returned to the manufacturer to assess post-exposure structural integrity. G6 sensors, which contain no electrical components or compressible air spaces, do not pose a risk in the hyperbaric environment. There was no observed change in preset EGVG readings during hyperbaric exposures. Post-exposure testing revealed no structural compromise after repeated hyperbaric exposures. The CGM transmitter meets section 14.2.9.3.17.5 of the 2018 NFPA 99 requirements for battery-operated devices allowed for use in a hyperbaric environment. This analysis revealed no significant safety concerns with subjecting Dexcom G6 CGM transmitters to hyperbaric environments.

The Role of Regional Cultural Values in Decisions about Hurricane Evacuation

This paper explores perceived risk within the context of regional cultural values. We describe aspects of local culture in Galveston, Texas, as emically defined, which affected response to a mandatory evacuation order for Hurricane Ike. Since over the past two decades about a third of residents failed to evacuate for hurricanes, we focused on understanding why residents would choose to stay. We used a matched-pair design to control for socioeconomic status and resources that might affect evacuation. Thus, pairs of neighbors were interviewed (one person who evacuated and a neighbor who did not evacuate). Using a new technique (qualitative comparative analysis) to find clustering among people and themes, narratives from in-depth open-ended interviews revealed two distinct groups of people with separate motivations for not evacuating. One group focused on the hazards of leaving because traffic hazards could be greater than storm risk, combining traffic risk with past experiences and concern about delay in reentering. These people were well-prepared with supplies and equipment to survive for a week or two without services. A second group focused on media “hype;” they simply did not believe news sources about the danger the storm posed. Unfortunately, in this case, the media warnings were correct, and the storm flooded the town with about thirteen feet of seawater, sewage, and debris. The historical pattern of official warnings, response actions, and media warnings considered to be “hype,” may actually be encouraging a culture of non-compliance with future mandatory evacuation orders.

Analysis of factors related to failure in the pressure test: a six-year experience in Taiwan

The Republic of China Navy instituted the pressure test as one of the selection tools for diving troops and submarine crews. We analyzed factors associated with failure in the pressure test. This was a retrospective cohort study designed to investigate pressure test failure in Navy recruits between January 2010 and August 2015. The recruits received pressurization in a hyperbaric chamber to a simulated depth of 112 feet of seawater (fsw) at a rate of 25 fsw/minute. Data describing trainee demographics, disease history, causes and depth of failure, as well as type of injury, were extracted from case notes and facility databases for statistical analysis. Of 3,608 trial cohorts, there were 435 failures, with an overall failure rate of 12.06%. About 95% of these failure trials were within a simulated depth of 60 fsw. Fifty-seven (57) failures did not record causes of failure. Among the other 378 failures, the most commonly identified causes were ear barotrauma (365 trials, 96.56%) and sinus barotrauma (10 trials, 2.65%). Statistical analysis revealed that recent upper respiratory tract infection, allergic rhinitis, and cigarette smoking were all significantly associated with higher incidence of middle ear barotrauma. Our results suggest that pressure testing to a depth of 60 fsw is effective in disqualifying personnel entering diving and submarine service. Recent infection of the upper respiratory tract, allergic rhinitis and cigarette smoking are risk factors for middle ear barotrauma, resulting in failure of the pressure test.

The effect of the perfluorocarbon emulsion Oxycyte on platelet count and function in the treatment of decompression sickness in a swine model.

Decompression from elevated ambient pressure is associated with platelet activation and decreased platelet counts. Standard treatment for decompression sickness (DCS) is hyperbaric oxygen therapy. Intravenous perfluorocarbon (PFC) emulsion is a nonrecompressive therapy being examined that improves mortality in animal models of DCS. However, PFC emulsions are associated with a decreased platelet count. We used a swine model of DCS to study the effect of PFC therapy on platelet count, function, and hemostasis. Castrated male swine (n = 50) were fitted with a vascular port, recovered, randomized, and compressed to 180 feet of sea water (fsw) for 31 min followed by decompression at 30 fsw/min. Animals were observed for DCS, administered 100% oxygen, and treated with either emulsified PFC Oxycyte (DCS-PFC) or isotonic saline (DCS-NS). Controls underwent the same procedures, but were not compressed (Sham-PFC and Sham-NS). Measurements of platelet count, thromboelastometry, and coagulation were obtained 1 h before compression and 1, 24, 48, 96, 168 and 192 h after treatment. No significant changes in normalized platelet counts were observed. Prothrombin time was elevated in DCS-PFC from 48 to 192 h compared with DCS-NS, and from 96 to 192 h compared with Sham-PFC. Normalized activated partial thromboplastin time was also elevated in DCS-PFC from 168 to 192 h compared with Sham-PFC. No bleeding events were noted. DCS treated with PFC (Oxycyte) does not impact platelet numbers, whole blood clotting by thromboelastometry, or clinical bleeding. Late changes in prothrombin time and activated partial thromboplastin time associated with PFC use in both DCS therapy and controls warrant further investigation.

Cardiovascular parameters in a mixed-sex swine study of severe decompression sickness treated with the emulsified perfluorocarbon Oxycyte.

Intravenous perfluorocarbons (PFC) have reduced the effects of decompression sickness (DCS) and improved mortality rates in animal models. However, concerns for the physiological effects of DCS combined with PFC therapy have not been examined in a balanced mixed-sex population. Thirty-two (16 male, 16 female) instrumented and sedated juvenile Yorkshire swine were exposed to 200 feet of seawater (fsw) for 31 min of hyperbaric air. Pulmonary artery pressure (PAP), cardiac output (CO), and systemic arterial pressure (SAP) were monitored before (control) and after exposure. Animals were randomized to treatment with Oxycyte (5 ml/kg; Oxygen Biotherapeutics, Inc., Morrisville, NC) vs. saline (control) with 100% oxygen administered upon DCS onset; animals were observed for 90 min. Parameters recorded and analyzed included PAP, CO, and SAP. In all animals PAP began to rise prior to cutis marmorata (CM) onset, the first sign of clinical DCS, generally peaking after CM onset. Female swine, compared with castrated males, had a more rapid onset of CM (7.30 vs. 11.46 min postsurfacing) and earlier onset to maximal PAP (6.41 vs. 9.69 min post-CM onset). Oxycyte therapy was associated with a sustained PAP elevation above controls in both sexes (33.41 vs. 25.78 mmHg). Significant pattern differences in PAP, CO, and SAP were noted between sexes and between therapeutic groups. There were no statistically significant differences in survival or paralysis between the PFC and control groups during the 48-h observation period. In conclusion, Oxycyte therapy for DCS is associated with a prolonged PAP increase in swine. These species and sex differences warrant further exploration.

Vigabatrin prevents seizure in swine subjected to hyperbaric hyperoxia

Oxygen is the most widely used therapeutic strategy to prevent and treat decompression sickness (DCS). Oxygen prebreathe (OPB) eliminated DCS in 20-kg swine after rapid decompression from saturation at 60 feet of seawater (fsw). However, hyperbaric oxygen (HBO) has risks. As oxygen partial pressure increases, so do its toxic effects. Central nervous system (CNS) oxygen toxicity is the most severe side effect, manifesting as seizure. An adjunctive therapeutic is needed to extend OPB strategies to deeper depths and prevent/delay seizure onset. The Food and Drug Administration-approved anti-epileptic vigabatrin has prevented HBO-induced seizures in rats up to 132 fsw. This study aimed to confirm the rat findings in a higher animal model and determine whether acute high-dose vigabatrin evokes retinotoxicity symptoms seen with chronic use clinically in humans. Vigabatrin dose escalation studies were conducted 20-kg swine exposed to HBO at 132 or 165 fsw. The saline group had seizure latencies of 7 and 11 min at 165 and 132 fsw, respectively. Vigabatrin at 180 mg/kg significantly increased latency (13 and 27 min at 165 and 132 fsw, respectively); 250 mg/kg abolished seizure activity at all depths. Functional electroretinogram and histology of the retinas showed no signs of retinal toxicity in any of the vigabatrin=treated animals. In the 250 mg/kg group there was no evidence of CNS oxygen toxicity; however, pulmonary oxygen toxicity limited HBO exposure. Together, the findings from this study show that vigabatrin therapy is efficacious at preventing CNS oxygen toxicity in swine, and a single dose is not acutely associated with retinotoxicity.

The emulsified perfluorocarbon Oxycyte improves spinal cord injury in a swine model of decompression sickness

A prospective, animal model for pharmacological intervention of decompression sickness (DCS), including spinal cord (SC) injury. Signs and symptoms of DCS can include joint pain, skin discoloration, cardiopulmonary congestion and SC injury; severity ranges from trivial to fatal. Non-recompressive therapy for DCS may improve time-to-treatment and therefore impact mortality and morbidity. Oxycyte at 5 cc kg(-1) provides both SC protection and statistically significant survival benefit in a swine model of DCS. The purpose of this study was to test whether a reduced dose of Oxycyte (3 cc kg(-1)) would provide similar benefit. Silver Spring, MD, USA METHODS: Male Yorkshire swine (N=50) underwent a non-linear compression profile to 200 fsw (feet of sea water), which was identical to previous work using the 5 cc kg(-1) dose of Oxycyte. After 31 min of bottom time, decompression was initiated at 30 fsw per minute until surface pressure was reached. Following decompression and the onset of DCS, intravenous Oxycyte or saline was administered with concurrent 100% O(2) for 1 h. The primary end point was DCS-induced mortality, with Tarlov score and SC histopathology as secondary end points. Oxycyte administration of 3 cc kg(-1) following surfacing produced no significant detectable survival benefit. Animals that received Oxycyte, however, had reduced SC lesion area. Further studies to determine the lowest fully efficacious dose of Oxycyte for the adjunct treatment of DCS are warranted.

The Study on Supply Air Pressure of Surface Supplied Diving System Based on Bernoulli’s Equation

Surface supplied air diving includes those forms of diving where air is supplied from the surface to the diver by a flexible hose. The Surface Supplied Diving Systems (SSDS) are used primarily for operations to 190 feet of seawater. For the safe of surface supplied diving operation, the gas flow and gas pressure of SSDS must be ensured. Based on the hydrodynamic equations of high-pressure gas hose flow, the basic equation for high-pressure gas flow of surface supplied diving system is analyzed, according to which the gas pressure, gas flow and umbilical basic parameters of surface supplied diving operation are affirmed.

High doses of pseudoephedrine taken 2 hours prior to “diving” to 132 feet of seawater (5 ATA) while breathing pure O2 increases risk for CNS oxygen toxicity in unanesthetized rats

Pseudoephedrine (PSE) salts (hydrochloride and sulfate) are commonly used as a decongestant by scuba divers. Anecdotal evidence collected by Divers Alert Network (DAN) suggests that use of PSE prior to making a high dose O2 dive (Nitrox or a rebreather using pure O2) increases the risk of CNS oxygen toxicity (CNS‐OT; i.e., seizures). We hypothesized that high doses of PSE reduces latency to seizure (LS) in unanesthetized rats breathing a lethal dose of HBO2 (5 ATA). Adult male rats were implanted with a radio‐transmitter for recording EEG, body temperature (TB), and activity. After ≥7 day recovery, a rat was given saline solution (control) or a dose of PSE hydrochloride intragastrically via gavage tube 2hr prior to “diving” (mg PSE/Kg): 0 (control), 80, 100, 120, 160 & 320 (9 rats/group). The rat was placed into a sealed chamber inside a hyperbaric chamber, which were pressurized in parallel with pure O2 and air, respectively, to 5 ATA until the onset of seizure. Our results show a significant dose dependent decrease in LS, compared to the control, at doses of 100–320 mg/Kg. We conclude that high doses of PSE should be avoided in deep dives breathing pure O2 as it increases the risk for CNS‐OT (DAN).

Serum Heat Shock Protein after Simulated Deep Diving in Navy Divers

Deep sea diving might cause a tremendous physical or psychological stress to the divers. The present study aims to evaluate the stress response to a simulated wet dive in Navy divers. Nineteen Navy divers took part in this study when they were undergoing annual deep dive training. Ten divers were exposed to 190 feet of sea water (fsw) breathing compressed air on day 1 and to 250 fsw breathing helium-oxygen (Heliox) gas mixture on day 3. Another 9 divers were exposed to 220 fsw on day 1 and 285 fsw on day 3 breathing Heliox gas mixture. The bottom time ranged from 5 to 8 min, and then the standard U.S. Navy air and Heliox decompression tables were followed for surfacing. Predive levels of serum heat shock protein 72 (sHsp72) were 9.95 +/- 0.56 ng/ml, which were significantly higher than those in the control group (8.01 +/- 0.77 ng/ml). After simulating Heliox dive, the sHsp72 increased to 10.43 +/- 0.56 ng/ml, but this was not statistically significant. Our results demonstrated that the serum level of Hsp72 is higher in the Navy divers who underwent regular intensive exercise. However, it remains unknown whether this increase of stress protein is associated with the diving stress or exercise preconditioning in the Navy divers.

Response

Response

Best Catch from NANOSNET

Best Catch from NANOSNET

Effects of hyperbaric exposure on the integrity of the internal components of commercially available cochlear implant systems.

This study investigated whether pressure changes common to scuba diving and to hyperbaric oxygen therapy would not cause crush damage or leakage from critical seals in commercially available cochlear implants. The implanted packages of cochlear implants are susceptible to electrical failure caused by leakage from critical seals and to crush injury when exposed to changing barometric pressures encountered in recreational diving and in hyperbaric oxygen therapy. Six Clarion 1.2, eight MED-EL Combi-40+, six Nucleus CI22M, and six Nucleus CI24M cochlear implants underwent three exposures at 165 feet of seawater (FSW) (6 ata abs), 99 FSW (4 ata abs), and 60 FSW (2.8 ata abs), simulating rates in accordance with U.S. Navy dive tables for nondecompression dives. Dives to 45 FSW (2.4 ata abs) simulated wound therapy. Before each dive began, after each dive, and after completion of the dive protocol, each device underwent telemetry and electrical integrity checks. All implants were returned to their respective factories for final electrical and quality control testing. All 26 devices completed the dive protocol. One Nucleus CI24M implant had a fault recorded at electrode lead 18 on predive and final product testing, which was absent during interval dive measurements. All 26 devices passed final electrical and quality control testing. In addition, the six Clarion units passed repeat helium leak testing. The implanted components of the Clarion 1.2, MED-EL Combi-40+, and Nucleus CI22M and CI24M were safely subjected to repeated pressure changes up to 6 atm abs, equivalent to 165 feet of seawater, without electrical failure from leakage at critical seals or crush damage.

Natural history of severe decompression sickness after rapid ascent from air saturation in a porcine model.

We developed a swine model to describe the untreated natural history of severe decompression sickness (DCS) after direct ascent from saturation conditions. In a recompression chamber, neutered male Yorkshire swine were pressurized to a predetermined depth from 50-150 feet of seawater [fsw; 2.52-5.55 atmospheres absolute (ATA)]. After 22 h, they returned to the surface (1 ATA) at 30 fsw/min (0.91 ATA/min) without decompression stops and were observed. Depth was the primary predictor of DCS incidence (R = 0.52, P < 0.0001) and death (R = 0.54, P < 0.0001). Severe DCS, defined as neurological or cardiopulmonary impairment, occurred in 78 of 128 animals, and 42 of 51 animals with cardiopulmonary DCS died within 1 h after surfacing. Within 24 h, 29 of 30 survivors with neurological DCS completely resolved their deficits without intervention. Pretrial Monte Carlo analysis decreased subject requirement without sacrificing power. This model provides a useful platform for investigating the pathophysiology of severe DCS and testing therapeutic interventions. The results raise important questions about present models of human responses to similar decompressive insults.