Decompression Sickness Treatment & Management
- Author: Stephen A Pulley, DO, MS, FACOEP; Chief Editor: Joe Alcock, MD, MS more...
Extricate the patient from water and immobilize if trauma is suspected.
Generally, in-water recompression is not believed to be a safe option. Problems with air supply, hypothermia, potential oxygen toxicity, dehydration, and the uncontrolled environment make it less than ideal and increase the risks of drowning. However, in remote areas without reasonable-distance hyperbaric oxygen (HBO) chamber support, this may be the only option. In Thailand, home to the diving Urak Lawoi fishermen, 72.1% exceed the no-decompression limits, yet medical treatment and HBO facilities are distant (10 h and 16 h, respectively). In this population, one third reported having experienced decompression sickness (DCS), and in-water recompression has been shown to be an appropriate first-aid measure. Much more research needs to be performed on the concept of in-water decompression, since over half of the Urak Lawoi (not just one third) were classified as experiencing recurring nondisabling DCS and about one quarter as having disabling DCS.[119, 120, 121] A shorter in-water recompression protocol was also developed for use in the remote Northern Pacific Clipperton Atoll in an attempt to address the above concerns. In-water recompression has been used successfully in a fishing population in Vietnam. Better outcomes were obtained when the recompression was done with oxygen instead of air.
Administer 100% oxygen, intubate if necessary, and intravenously administer saline or lactated Ringer solution.
The use of first aid oxygen has proven so beneficial that the Divers Alert Network (DAN) has made a major effort to place oxygen at dive locations, in particular those that are remote with lengthy transport times to the nearest hyperbaric chambers and to ensure that people are trained in its use. A study of the use of first aid oxygen found that the median time to its use after surfacing was 4 hours and 2.2 hours after the onset of DCS symptoms. Forty-seven percent of victims received the oxygen. Complete relief of symptoms was found in 14% of victims. Even more striking was that 51% of victims showed improvement. This was with the oxygen before HBO treatment. Even after a single HBO treatment, those that had received oxygen before the HBO dive, even if many hours earlier, had better outcomes.
Aspirin is commonly considered and given in diving accidents for antiplatelet activity if the patient is not bleeding. However, there are no current data to support this practice. The nitrogen bubbles interact with platelets, leading to adhesion and activation, which is thought to contribute to micro venous obstruction and resultant ischemia in DCS; however, no studies or trials of the effect or benefit of aspirin on this process have been conducted. Giving aspirin could increase bleeding, especially in severe DCS.[125, 126, 127]
Thus far there is no substantive data showing a benefit for other adjunctive treatments, such as recompression with helium/oxygen and NSAIDs.
Perform cardiopulmonary resuscitation and advanced cardiac life support, if required, as well as needle decompression of the chest if tension pneumothorax is suspected.
Do not put the patient into the Trendelenburg position. Placing the patient in a head-down posture used to be considered a standard treatment of diving injuries to prevent cerebral gas embolization. This practice should be abandoned. The process actually increases intracranial pressure and exacerbates injury to the blood-brain barrier. It also wastes time and complicates movement of the patient.
Transport to the nearest emergency department and hyperbaric facility, if feasible, and try to keep all diving gear with the diver. Diving gear may provide clues as to why the diver had trouble (eg, faulty air regulator, hose leak, carbon monoxide contamination of compressed air).
Emergency Department Care
Administer 100% oxygen to wash nitrogen out of the lungs and set up an increased diffusion gradient to increase nitrogen offloading from the body.
Do not put the patient into the Trendelenburg position. Placing the patient in a head-down posture used to be considered a standard treatment of diving injuries to prevent cerebral gas embolization. This practice should be abandoned. The process actually increases intracranial pressure and exacerbates injury to the blood-brain barrier. It also wastes time and complicates movement of the patient.
Perform intubation and aggressive resuscitation including advanced cardiac and trauma life support. Be alert for the potential of tension pneumothorax and perform needle decompression followed by chest tube thoracostomy, if indicated. Also be aware of the potential for pneumoperitoneum from ruptured viscus. The air collection can be so great as to interfere with hemodynamics. Emergent needle decompression of the peritoneum is the corrective procedure.
Administer intravenous fluids for rehydration until urinary output is 1-2 mL/kg/h. Rehydration improves circulation and perfusion.
Aspirin is commonly considered and given in diving accidents for antiplatelet activity if the patient is not bleeding. However, there are no current data to support this practice. The nitrogen bubbles interact with platelets, leading to adhesion and activation, which is thought to contribute to micro venous obstruction and resultant ischemia in DCS. However, no studies or trials of the effect or benefit of aspirin on this process have been conducted. Giving aspirin could increase bleeding, especially in severe DCS.[125, 126, 127]
Treat the patient for nausea, vomiting, pain, and headache.
Contact the closest hyperbaric facility (or DAN for referral) to arrange transfer and try to keep all diving gear with the diver. The diving gear may provide clues as to why the diver had trouble (eg, faulty air regulator, hose leak, carbon monoxide contamination of the compressed air).
Patients with type I or mild type II DCS can dramatically improve and have complete symptom resolution. This improvement should not dissuade the practitioner from HBO referral or transfer, as relapses have occurred with worse outcomes.
Diving medicine and HBO specialists
Symptoms temporally related to diving should necessitate a consultation with a diving medicine or HBO specialist to determine if symptoms are related to diving and if HBO therapy is appropriate.
Divers Alert Network
Divers Alert Network is an excellent resource, especially if local support is not available. While their emergency contact numbers are below, visit their Web site at International DAN or IDAN for the full contact information. Use of this service is similar to use of a poison control center. DAN maintains a database of diving-related injuries and provides consultation services, including extent-of-injury assessment, recommendations for management, and referral to HBO therapy or local diving medicine specialists. Emergency contact 24 hours per day can be reached at the following numbers:
DAN World[wide] Emergency Number: +1-919-684-9111 (accepts collect calls)
DAN America Emergencies: +1-919-684-9111 (accepts collect calls); nonemergency: +1-919-684-2948
DAN Brasil Emergencies: +1-919-684-9111 (accepts collect calls); in Brasil: 0800 684 9111
DAN Europe Emergencies: +39-06-4211-8685; nonemergency: +39-085-893-0333
DAN Southern Africa Emergencies: 0800-020-111 (within South Africa); +27-828-10-60-10 (outside South Africa, accepts collect calls); nonemergency: 0860-242-242, +27-11-266-4900
DAN Japan Emergencies: +81-3-3812-4999; nonemergency: +81-45-228-3066
DES Australia: 1-800-088-200 (toll free within Australia—English only); +61-8-8212-9242 (from outside Australia—English only)
DES New Zealand: 0800-4DES-111 (within New Zealand—English only)
Korean Hotline: 010-4500-9113 (Korean and English)
Note: Numbers do change from time to time. See https://www.diversalertnetwork.org/contact/international.asp for the latest list.
Again, acute DCS is a purely clinical diagnosis that requires a fair amount of clinical suspicion. When the slightest suspicion or possibility is noted, timely transfer with 100% FIO 2 oxygen for HBO should be pursued. Accessing consultation as discussed above is advised if any confusion or concerns are noted.
Patients with mild type I DCS probably do not require treatment other than breathing pure oxygen at sea level for a short time. However, as discussed with regard to inner-ear DCS (IEDCS) and cutis marmorata, there are newer theories that they are more serious and they should be considered for HBO therapy. Divers with type I DCS symptoms do, however, require close observation, as symptoms may portend the onset of more serious problems requiring hyperbaric recompression. Consult a diving medicine or HBO specialist for all diving-related injuries. The only effective treatment for gas embolism is recompression; other treatments are merely for symptoms.
Several types of hyperbaric chambers exist, ranging from small monoplace (single person) chambers to complex multiple place, multiple lockout chambers large enough for multiple patients and attendants. All chambers have the ability to maintain critical care monitoring and mechanical ventilation. A major difference with the size of chambers clinically is that some patients experience claustrophobia with the small monoplace chambers. Increased oxygen toxicity issues have been reported with the monoplace chambers because the entire environment is oxygenated, whereas, with the larger chambers, patients breathe the oxygen via mask, but the ambient environment is not supplementally oxygenated. In addition, the ability of attendants to be in with the patient allows for resuscitation or other intensive treatment in the sickest of patients. The number of hyperbaric chambers across the United States has increased rapidly as the therapy is used for many clinical entities ranging from wound care to multiple sclerosis. However, of 361 chambers contacted and interviewed nationwide, only 43 were judged to have the equipment and staff to treat high-acuity patients. This was thought to be an inadequate number for the United States.
The basic theory behind HBO therapy is to first repressurize the patient to simulate a depth where the bubbles from nitrogen or air are redissolved into the body tissues and fluids. Then, by breathing intermittently higher concentrations of oxygen, a larger diffusion gradient is established. The patient is taken slowly back to surface atmospheric pressure. This allows gases to diffuse gradually out of the lungs and body. The addition of helium to oxygen has been shown to yield an advantage over oxygen alone even in severe neurologic DCS or treatment-refractory DCS.[131, 132]
Treatment tables govern the exact combination of timing and depths. These were developed primarily by the US Navy with some minor modifications by the US Air Force. Table 6 is most commonly used. However, specific details concerning the tables are beyond the scope of this article. While most will improve with a single HBO treatment, 38.5% will have relapses, half of those within 24 hours. Observation for 24 hours is strongly recommended after HBO treatment. Another study reported complete resolution of symptoms in 49% with the first treatment and an additional 26.5% with additional treatments. However, 24.5% had long-term residual symptoms. In Israel, 48% had complete recovery with HBO, while another 48% had partial recovery. Unfortunately, 4% did not respond to the therapy. Yet, HBO effectiveness rates as high as 99% have been reported.
Delay to treatment has long been felt to yield worse outcomes. More recent studies conflict with that traditional thinking. In one study, a longer delay to treatment was related to incomplete recovery but the increased risk appeared negligible. In another, delays in treatment of longer than 17 hours could not be correlated with increased number of HBO treatments or worse outcome in DCS. Instead, the severity of the neurologic dysfunction and rapid onset of symptoms after surfacing were the main factors in predicting the severity of DCS and the resistance to treatment with worse outcomes.[27, 28, 136] In Israel, they specifically looked at delayed recompression defined as greater than 48 hours. They found no significant difference in outcome between early and delayed treatment groups. Complete recovery occurred in 78% versus 76%, respectively; partial recovery occurred in 15.6% versus 17.1%, respectively; and no improvement occurred in 6.2% versus 6.6%, respectively.
Traditionally, the treatment protocols were staged, meaning that time would be spent at certain depths as the individual was "brought back to the surface." Recent studies suggest that a linear approach is more effective than the staged approach. Other variations on the tables are being researched to try to find shorter-term approaches. In addition, use of combination gases, such as Trimix, are being looked at in the same regard. Another mentioned adjunct to HBO includes negative-pressure breathing.
An interesting area of research relates to the use of intravenous perfluorocarbon (PFC) emulsions.[139, 140] PFCs are synthetic liquids made up of carbon and fluorine that has the ability to dissolve significant amounts of gases especially oxygen. As they are hydrophobic, they have to be emulsified in order to use them intravenously in water based organism such as humans. This is being studied as a temporary blood substitute in numerous clinical settings. It is being studied in the setting of the treatment of DCS in conjunction with HBO therapy.
One such PFC, trade name Oxycyte, has been shown to provide protection and improve outcomes in spinal DCS at 5 mL/kg IV. Improved oxygenation is the presumed mechanism.[142, 143, 144] PFCs appear to decrease DCS symptoms through a combination of decreasing bubble formation, hemodynamic protection against gas embolism, enhanced oxygen delivery to tissues, and increased pulmonary nitrogen washout (this last effect is hypothesized but not shown).[145, 146] There was concern for decreased platelet counts as both decompression and PFCs appeared to cause that decrease. Oxycyte PFC was not found to affect platelets or clotting or bleeding. The positive effects of PFCs are further enhanced by oxygen prebreathing (before HBO treatment) with increased oxygen delivery.
With early recognition and treatment more than 75% of patients improve. Even with significant delays in recognition and treatment, positive results are obtained.[149, 150] Studies of the Miskito Indians of Central America highlight this. They are diving seafood harvesters who dive repeatedly without consideration for diving tables or profiles. They have a high prevalence of the bends and neurologic DCS that affects the thoracolumbar spine in particular. Despite very high rates of DCS, and sometimes days' delays in HBO treatment (if sought at all), HBO treatment yields positive results, with 30% regaining strength and many more ambulating. However, HBO treatment is usually only sought for significant neurologic symptoms, while painful DCS, such as the bends, is usually treated with only analgesia.[151, 152]
Differentiating inner ear barotrauma or dysbarism from inner ear labyrinthine or alternobaric vertigo is difficult. The difference is that dysbarism responds well to treatment, and inner ear DCS is less responsive and is associated with a higher frequency of permanent damage. Patients with inner ear DCS may be asymptomatic after treatment yet still have vestibular problems at detailed testing. Therefore, both conditions must be considered in the differential diagnosis, and the patient must be treated for both conditions. One recommendation is to perform immediate tympanocentesis and then to follow with HBO therapy. IEDCS is less responsive to HBO treatment than is DCS affecting other sites. Incomplete recovery has been reported in 68% of those receiving HBO therapy. HBO typically results in significant improvement in severe neurologic DCS if it is identified early and the patient is rapidly transported to an HBO facility.
Rapid treatment is also crucial in the face of arterial gas embolization (AGE). Those with AGE who reach recompression within 5 minutes have a death rate of only 5%. This rapid treatment also results in little morbidity. However, when AGE recompression is delayed 5 hours, the mortality rate approaches 10%. More than 50% of the survivors experience residual signs.
Transfer to a hyperbaric facility is strongly advised. An important issue is timely transport of the patient to the closest hyperbaric facility. This is frequently accomplished by land transport; however, air transportation is occasionally required. An effort should also be made to minimize the transport time. This is frequently accomplished by land transport; however, air transportation is occasionally required. Helicopter transport requires the pilot to maintain an altitude of less than 500 ft (152 m) above the departure point (which could be more than 500 ft above sea level depending on the dive location). This can be difficult when there are mountains to traverse in flight. In this situation explore options other than rotary-wing transportation to the closest chamber. An effort should also be made to minimize the transport time. Fixed-wing transport should be limited to aircraft that can maintain cabin pressure at normal surface pressure of 1 atm (eg, Lear Jet, Cessna Citation, and military C-130 Hercules).
Key to preventing DCS is exercising conservatism in the diving profile and always putting safety first. Education is key in this regard. In Vietnam, severe DCS was decreased by 75%, and mortality also dropped, after a concerted educational effort. Even with education and a conservative approach, DCS can still occur. The total amount of saturated nitrogen was thought at one time to be the primary determinant of an individual's risk of developing DCS. Thus, the diving tables reflected close attention to the time spent at depths and surface intervals for repetitive dives. Further research and thought suggests that the rate of ascent from depths may be a more critical factor.[84, 85]
Early diving instruction recommended a rate of ascent no faster than 60 ft (18 m) per minute. The more recent recommendation was to ascend no faster than 30 ft (10 m) per minute and to make a 3- to 5-minute safety stop at 15-20 ft (4.6-6 m).[154, 155] Therefore, the time of ascent was increased for a 60-ft dive from 1 minute to a maximum of 7 minutes.
Doppler bubble research has revealed that the release of bubbles from tissues is a critical factor in the development of DCS. The tissues that appear to saturate the fastest are in the spinal cord, with maximum saturation occurring in as few as 12 minutes. Desaturation, or off-gassing, is much slower. Thus, even a no-decompression dive at 60 ft (20 m) for 20 minutes maximally saturates spinal tissues. As mentioned earlier, these are the tissues most commonly affected in type II DCS.
Even the slower 7-minute ascent to reach the surface from a 60-ft (20 m) dive still leaves a sizable amount of dissolved nitrogen in the faster-saturating spinal tissues. The remaining nitrogen can then bubble even on this slower ascent.
According to DAN, data from a European study revealed that increasing this ascent time to 18 minutes eliminated the dangerous bubbles. Therefore, one or more additional stops at deeper level(s) are likely needed to lengthen ascent time adequately and thus protect against DCS. Research has shown that a safety stop of 2.5-5 minutes at 50 ft (15 m) in addition to another stop at 20 ft (6 m) for 3-5 minutes decreases venous bubble formation at least for a no-decompression dive of 82 ft (25 m). The supposition here is that this can decrease the risk of DCS. Obviously, this requires that more of the air reserve is allotted for the ascent. In addition, premeasured, weighted ropes attached to the diving platform for the set safety stops can help maintain the desired depth and prevent drifting away from the surface vessel. Additional scuba tanks could be added at each safety level in case diver air supplies reach a critical level.
Breathing 100% fraction of inspired oxygen (FIO2) oxygen during the decompression stops may help prevent DCS. One should consider the partial pressure of oxygen at the decompression stop depth to prevent toxicity. Being active during the decompression stops may also decrease the likelihood of bubble formation.[157, 158, 159]
Close attention to adequate hydration before and immediately after a dive may also have protective effects. The mechanism is discussed under Pathophysiology. In an individual with normally functioning kidneys, the frequency of urination and the concentration color of the urine are easy indicators of whether sufficient fluids are being taken in. A long time between urinating and a deep color are signs of inadequate intake. Note that these fluids should not be heavily caffeinated and should be alcohol free.
The culture of diving, at least in military naval diving, may have some impact on prevention of diving accidents. The two most common causes of naval diving accidents, or near misses, were leadership failures and decreased situational awareness. These came into play when the overall risk was underestimated and the time was not closely monitored. In addition, the need for junior divers to ask questions was rebuffed by the posture of the senior divers not being interested in providing answers. While this was found in the US Navy, correlations could be considered in the average dive situation, namely daily dive charters. A lack of leadership, in the form of a dive master, and the generally isolated situation of a number of divers not knowing each other, could lead to the same overall environment.
When an air bubble expands within a normally air-containing structure such as ears, sinuses, lungs, and GI system, a problem emerges. Another issue is when nitrogen that is saturated in tissues and blood expands with decreasing pressure. Normally, it returns to the lungs and is exhaled. It does not have any other ready exit to the outside. When the bubbles occur, they cannot be exhaled from the lungs and can interfere with blood flow directly causing ischemia, or their expansion in tissues causes dysfunction of those tissues and if in a sensory nerve‒containing area, such as the synovium of the joints, can cause pain. This causes DCS. However, another mechanism is also at work. That is the interaction between the bubbles and the normal blood clotting system. The interface causes clot formation and inflammation, which further increases ischemia and dysfunction.
To this point, the major way to avoid this bubbling has been through conservative diving using tables or computers that are based on the experiences of fit military divers. By staying within the table parameters, it was hoped that excessive tissue nitrogen saturation could be avoided so that it would not come out of solution as bubbles on ascent. Computer models are being validated that may lead to more accurate determination of these tables. The next step in the process to avoid DCS was to ascend slowly. The recommended ascent rate has decreased steadily, as mentioned above, to the point where the recommendation is to stop ascent at decompression stops to allow the exhalation of nitrogen gas, rather than it bubbling in the blood.
Despite these measures, individuals with similar body types and diving the same profiles resulted in some getting DCS and others not. The hope is that further research will decrease the risk and incidence of DCS.
The gas nuclei and nitrogen interface appear to be key in better prevention strategies regarding DCS. In particular, the protection appears to be related to nitric oxide and nitric oxide synthase. A progression of studies from rats to trained, fit, military divers and now in experienced recreational divers is showing that inhibiting nitric oxide synthase increases the number and sizes of bubbles and that administering a nitric oxide donor decreases the number and size of bubbles. This effect occurred with a long-acting agent at 20 hours and 30 minutes before the dive.
More recently, a short-acting nitric oxide donor, the common sublingual medication nitroglycerin (0.4 mg), administered 30 minutes prior to a dive, was found to provide this same level of protection by decreasing bubble formation. Because it is arginine and oxygen that are converted by nitric oxide synthetase to nitric oxide, one might surmise that taking the common L-arginine amino acid would help drive the equation to nitric oxide. Caution is advised as this has not been studied in this realm. In relation to erectile dysfunction, nitric oxide plays a role in erection. Apparently, significant improvement has not been found and it is hypothesized that some other mechanism prevents it.
Toxic effects of oxygen under pressure have also been studied. Oxidation and free radicals may also be important instigating factors. It causes vasoconstriction, which causes ischemia, activation of the inflammation cascade, and subsequent damage to the vascular endothelium. Antioxidants, maintaining normal hemostasis, and preventing inflammatory responses may help stop the DCS process from starting. After a DCS neurologic injury, many (about 30%) have incomplete recovery despite appropriate management. Inflammatory changes are believed to be at least part of the reason. Several substances have been studied in this realm, and preliminary data suggest that they may be useful. Fluoxetine, a common antidepressant medication in the serotonin-specific reuptake inhibitor (SSRI) class, has been found to decrease the incidence of DCS and improve motor function recovery by the limiting the inflammatory process. Based on rat models, it is believed to decrease inflammation through cytokine interleukin 10 suppression. Ascorbic acid 2 g daily for 6 days before a dive decreased neutrophil activation and microparticle generation. Simvastatin has been found to decrease the incidence of DCS in a rat population through its anti-inflammatory properties. Again, the reader is cautioned about taking any substance with the end goal of decreasing DCS until more advanced studies are completed and the individual has discussed their use with a physician well versed in diving medicine.
Another significant event has been the discovery of the positive benefit of a period of aerobic exercise at around 80% of maximal oxygen uptake in humans and 85-90% in rats. The timing of this exercise appears to be key. A period of exercise of 90 minutes in rats and 40 minutes in humans timed at 20 hours and 24 hours, respectively, before the dive, was found to have significant long-lasting effects on the number and size of nitrogen bubble formation.[168, 169, 170, 171] When the same exercise is completed at 2 hours and 30 minutes prior to the dive, the results are less clear. In some groups, a benefit was noted; in others, no benefit was noted.[172, 173] The exercise at 24 or 2 hours predive appears to affect bubble formation as it has no effect on enhancing nitrogen washout. It also did not decrease the median number of circulating venous gas emboli.
In one study, it was demonstrated that the positive effect of the exercise the day before was eliminated by a second period of exercise prior to the dive. It has also been demonstrated that it is not the overall level of fitness, but rather the timing of the exercise that provided the protection. This level of protection appears to be similar to that offered by the nitric oxide donor.[176, 177] The next step is to see exactly what biochemical effects the exercise causes. Nitric oxide appears to be the protective agent in the predive exercise.
Regular exercise, physical conditioning, and diving also appear to have a protective effect against bubble formation and DCS.
Postdive activity and exercise is controversial. Intense activity after a dive was believed to promote bubble formation. In small studies on trained, fit, military divers, a positive benefit has been found for mild exercise, at 30% of maximal oxygen uptake, during the 3-minute decompression stop on ascent. Other studies incorporating similar aerobic exercise, at 80% of maximal oxygen uptake, starting at 30 minutes and 40 minutes post dive, have failed to demonstrate any adverse effects on trained, fit, military divers. Postdive exercise is believed to dilate intrapulmonary arteriovenous anastomoses. This allows for a mechanism of right-to-left shunt and thus arterialization of the venous gas emboli (bubbles). As a result, the incidence of DCS increases.
So, the question is, what should the average diver do, or not do, based on the research?
As with anything in medicine, broad recommendations can only be reached after a sufficient number of large studies show benefit. This level of evidence has not yet been reached in the diving literature. Medical recommendations cannot be made from a textbook chapter because the knowledge has to be applied with consideration of the individual. Consultation with a physician experienced and knowledgeable in diving medicine is strongly advised.
Clearly, the benefit of aerobic exercise the day prior to a dive is evident. For the many recreational divers who are relatively sedentary as they fly long distances to remote areas and then start diving soon after arrival, this may have important consequences.
As with any physical activity, including scuba diving, the person must be physically fit before engaging in a stressful activity. This means being aerobically conditioned. This should be completed in consultation with a physician, in particular one with experience with the recreational activity.
All medications should only be taken on the recommendation of a physician who is familiar with the patient and the patient’s health history and only after consideration of the risks and benefits of the medication. In this specialized, off-label use, a specialist in diving medicine should be the consultant. Nitroglycerin is mentioned above. Nitroglycerin has many adverse effects, such as dilation of blood vessels, lowering of blood pressure, and headaches. Others also mentioned are L-arginine, fluoxetine, ascorbic acid, and simvastatin, with the same caution advised for all.
A period of prebreathing normobaric (regular oxygen bottle) oxygen for 30 minutes was found to decrease venous bubble formation for the subsequent dive and repetitive dives afterwards with no further prebreathing.[125, 180] In swine models, prebreathing oxygen at depth for as little as 5 minutes before rapid decompression helped prevent type II DCS; when breathed for 15 or 45 minutes, it decreased type I DCS symptoms. It also was found in swine models to decrease venous ischemia and osteonecrosis from DCS. In a rat model, oxygen prebreathing was not found to decrease DCS, but was found to decrease inflammatory reactions, and protein infiltration, in lung tissue. As with the statement about nitroglycerin above, oxygen is a medical gas and its use needs to prescribed by a physician. Also, if oxygen were to be used at depth, the toxic effects of partial pressures of oxygen must be considered.
In addition, a 30-minute predive sauna session at 65ºC (149ºF) was shown to decrease venous bubble formation, although the mechanism was not known. Nowadays, the mechanism is being demystified. A heat stress of 45ºC/113ºF for 1 hour decreased nitric oxide synthetase activity. It potentiates heat stress protein (HSP)70 and decreased HSP90. Glutathione (GSH) activity was found inversely related to the nitric oxide synthetase activity. The protective effects of HSP70 are believed to be related to the antioxidation and antiapoptosis. In contrast to this, being warm during the bottom portion of a dive actually increases nitrogen uptake, whereas being cool during that phase dive decreases uptake. On ascent, the reverse is true. Being warm on ascent increases off-gassing of nitrogen, while being cool delays this process. In this modern age of dry suits and suit warmers, one might be tempted to manipulate the temperature to be cool on descent and at the bottom and warm on the ascent. One is cautioned against doing this, as being too cool at the bottom can inhibit overall functioning and being too warm on ascent can promote localized gas bubbling.[106, 107]
What to do after the dive is less clear and needs more investigation in less-fit populations. Although the research appears promising that exercise after diving does not have an adverse effect and that some benefit may exist, the research is insufficient to recommend any changes.
A puzzling situation is when an individual experiences DCS when all facets of the dive appeared normal and highly conservative. This prompted a search for other possible influencing etiologies. The identification of the injured diver’s thrombotic state was found to be a possible explanation.
A high percentage of the unexplained DCS injured divers were found to have moderate increases in total plasma homocysteine, a substance found to be implicated in the formation of atherosclerosis (hardening of the arteries), and deficiencies in folate and vitamin B-12, common nutritional substances.[187, 188] These three chemicals are easily screened for with common laboratory testing. Correction of folate and B-12 deficiencies are easily treated with vitamin supplementation. Studies suggest that the homocysteine level increase can be treated favorably with folate and vitamin B-6 supplements. Again, this should also be completed under the advice of a physician.
Current research is aiming at fine-tuning the prevention of DCS. Transcranial, precordial, and subclavian vein Doppler examination; echocardiography; and regular ultrasonographic imaging have been used to detect the presence of bubbles in the vascular system of the volunteers being studied.[151, 189, 190] At the same time, various HBO decompression models are being evaluated using the same studies.[191, 192] As the database expands across the full spectrum of divers (not just young, healthy divers), the tables and recommended dive profiles continue to improve. However, since people respond differently to DCS, a universal profile is unlikely to be established. For this reason, all divers should fully understand their dive profiles (especially if generated by computer) and should always be conservative and allow plenty of room for individual variation and error.
Future trends are promising. Efforts are underway to identify specific biomarkers for DCS. S-100B is a sensitive biomarker being studied in brain injury in general and neurologic DCS specifically. Serum procalcitonin has been suggested as a potential decompression stress biomarker. Endothelial damage is theorized to increase permeability and inflammatory cytokines, leading to the elevated levels. D-dimer is a biomarker for activation of coagulation. In combination with a severity score, it improved judging of the severity in neurological DCS. Lactate dehydrogenase (LDH) is a marker of cell injury that has been used in decompression research.
Increased hematocrit has been correlated with hydration status after diving. The importance of being well hydrated has already been discussed as a risk factor in DCS. Platelet count decreases can correlate with increased platelet aggregation. This is one of the contributing causes of DCS.
A medication class with an adverse effect was found in the studies. Sildenafil (Viagra), a phosphodiesterase-5 blocker, was found to promote the onset and severity of neurological DCS. It is a potent smooth muscle relaxation vasodilator that is used in erectile dysfunction. Several medications are available in this class. Of note is that there are pulmonary hypertension medications in this same class. Many divers engage in diving while on vacation, when sexual activity may increase. Many of these medications are available without a prescription in other countries; thus, divers must be aware of the potential for this class to worsen DCS and thus avoid their use before diving. The half-lives of these medications range from 4 hours for sildenafil and vardenafil (Levitra) to 17.5 hours for tadalafil (Cialis). Clearance of a medication from the body requires 4-5 half-lives. Thus, the time to clear sildenafil and vardenafil would be 16-20 hours and for tadalafil it would be 70-87.5 hours, about half of a one-week vacation. Numerous common medications can prolong the effects of these medications. A diver prescribed one of these medications should discuss their use with the prescribing physician and consider consultation with a diving medicine specialist.
Closure of documented right-to-left shunt appears to prevent both symptomatic DCS and asymptomatic brain ischemia.[72, 199] However, routine screening of all divers is not recommended. Also controversial is prophylactic transcatheter closure of a patent foramen ovale (PFO) without documented DCS. As mentioned earlier, only large PFOs appear to greatly increase the risk in diving. The complication rate for this procedure is about 1%, which is much greater than the incidence of developing serious neurologic DCS. A proper medical approach to everything is to balance risk versus benefit. In this case, the weight appears to angle more towards risk. A better approach is to screen those divers who have developed DCS of the cerebral, spinal, inner-ear, and cutaneous types. Also for consideration would be divers with a history of migraine with aura and ischemic strokes (especially if younger). The screening study is agitated saline echocardiography under strict protocol, with meticulous technique and provocative maneuvers.[200, 201, 202] Those individuals found to have a PFO should then consult closely with a diving medicine specialist. It may be that using the strategies mentioned in this article in a very conservative manner is a better approach to mitigate risk than would be a recommendation for a surgical procedure. If the later procedure is chosen, the patient must be rescreened to ensure that the closure was complete.[59, 203, 204]
Delaying significant changes in altitude and resultant decreases in barometric pressure for 24 hours after the last dive had been a recommended strategy. This could include flying or ascending a mountain. However, in one study using inflight transthoracic echocardiography, 8 (14%) of 56 study participants who followed the 24-hour recommendation still had bubbles during the return flight. Therefore, a longer interval between the last dive and flying (eg, 36 h) may be more appropriate.
Finally, to add to the mix of influencing factors, diet has been found to have an adverse effect on the risk of developing DCS. Previously mentioned were specific nutritional deficiencies, including folate and vitamin B-12. Hydration status is also important. Now, meals high in cholesterol and triglycerides have been identified as increasing the risk for DCS.
A summary of protective strategies is as follows:
Good aerobic conditioning through regular cardiovascular exercise
Exercise 24 or 2 hours prior to diving
Hot environmental exposure prior to diving
Ensure good hydration before and after the dive
Prebreathing 100% FIO 2 oxygen predive
Regular diving has a protective acclimatization effect
A slow ascent with more than one decompression stop, with (1) breathing oxygen during decompression stops and (2) being active (but not excessive exercise) during decompression stops
Allow for a period of 24-36 hours after the last dive prior to flying or high-altitude ascent
Avoid high-fat meals prior to diving
With a history of prior DCS, the following is recommended:
The decision to continue diving must be made in consultation with a diving medicine specialist
If prior DCS is noted, with or without a right-to-left shunt, adopting a highly conservative dive profile greatly decreases the risk or DCS recurrence [199, 205]
To prevent recurrent DCS, the use of oxygen-enriched breathing mixtures may help  ; again, caution is advised related to oxygen partial pressures at depth and the potential for oxygen toxicity
Although specific medications were mentioned above, individual recommendations cannot be made. Any medication that is taken related to diving should be done in consultation with a diving medicine specialist.
A patient with DCS is most likely not discharged from the emergency department to outpatient care. Patients can dramatically improve or have complete resolution in type I or mild type II DCS with just oxygen and rehydration. However, this improvement should not dissuade the practitioner from diving medicine or HBO specialist consultation and referral or transfer for HBO, as relapses have occurred with worse outcomes. Therefore, referral to a hyperbaric facility is strongly advised.
Auten JD, Kuhne MA, Walker HM 2nd, Porter HO. Neurologic decompression sickness following cabin pressure fluctuations at high altitude. Aviat Space Environ Med. 2010 Apr. 81(4):427-30. [Medline].
AIDA International. World Records. Association Internationale pour le Développement de l'Apnée. Available at https://www.aidainternational.org/competitive/worlds-records. Accessed: March 17, 2014.
John Liang. Herbert Nitsch Speaks To DeeperBlue.com About His Recovery From His 2012 Dive Attempt. Deeper Blue. Available at http://www.deeperblue.com/herbert-nitsch-speaks-deeperblue-com-recovery-2012-dive-attempt/. Accessed: March 17, 2014.
Camporesi EM. Diving and pregnancy. Semin Perinatol. 1996 Aug. 20(4):292-302. [Medline].
Lemaitre F, Carturan D, Tourney-Chollet C, Gardette B. Circulating venous bubbles in children after diving. Pediatr Exerc Sci. 2009 Feb. 21(1):77-85. [Medline].
Blatteau JE, Souraud JB, Gempp E, Boussuges A. Gas nuclei, their origin, and their role in bubble formation. Aviat Space Environ Med. 2006 Oct. 77(10):1068-76. [Medline].
Thom SR, Milovanova TN, Bogush M, Bhopale VM, Yang M, Bushmann K, et al. Microparticle production, neutrophil activation, and intravascular bubbles following open-water SCUBA diving. J Appl Physiol (1985). 2012 Apr. 112(8):1268-78. [Medline].
Møllerløkken A, Breskovic T, Palada I, Valic Z, Dujic Z, Brubakk AO. Observation of increased venous gas emboli after wet dives compared to dry dives. Diving Hyperb Med. 2011 Sep. 41(3):124-8. [Medline].
Swan JG, Wilbur JC, Moodie KL, Kane SA, Knaus DA, Phillips SD, et al. Microbubbles are detected prior to larger bubbles following decompression. J Appl Physiol (1985). 2014 Apr. 116(7):790-6. [Medline].
Vallee N, Meckler C, Risso JJ, Blatteau JE. Neuroprotective role of the TREK-1 channel in decompression sickness. J Appl Physiol (1985). 2012 Apr. 112(7):1191-6. [Medline].
Bao XC, Fang YQ, Ma J, Meng M. [Change of adhesion molecules in the lungs of rat with decompression sickness]. Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2012 Jul. 28(4):369-72. [Medline].
Thom SR, Bennett M, Banham ND, Chin W, Blake DF, Rosen A, et al. Association of microparticles and neutrophil activation with decompression sickness. J Appl Physiol (1985). 2015 Sep 1. 119 (5):427-34. [Medline].
Yang M, Barak OF, Dujic Z, Madden D, Bhopale VM, Bhullar J, et al. Ascorbic acid supplementation diminishes microparticle elevations and neutrophil activation following SCUBA diving. Am J Physiol Regul Integr Comp Physiol. 2015 Aug 15. 309 (4):R338-44. [Medline].
Thom SR, Yang M, Bhopale VM, Milovanova TN, Bogush M, Buerk DG. Intramicroparticle nitrogen dioxide is a bubble nucleation site leading to decompression-induced neutrophil activation and vascular injury. J Appl Physiol (1985). 2013 Mar 1. 114(5):550-8. [Medline].
Pontier JM, Gempp E, Ignatescu M. Blood platelet-derived microparticles release and bubble formation after an open-sea air dive. Appl Physiol Nutr Metab. 2012 Oct. 37(5):888-92. [Medline].
Philp RB, Freeman D, Francey I, Bishop B. Hematology and blood chemistry in saturation diving: I. Antiplatelet drugs, aspirin, and VK744. Undersea Biomed Res. 1975 Dec. 2(4):233-49. [Medline].
Pontier JM, Blatteau JE, Vallée N. Blood platelet count and severity of decompression sickness in rats after a provocative dive. Aviat Space Environ Med. 2008 Aug. 79(8):761-4. [Medline].
Pontier JM, Jimenez C, Blatteau JE. Blood platelet count and bubble formation after a dive to 30 msw for 30 min. Aviat Space Environ Med. 2008 Dec. 79(12):1096-9. [Medline].
Blatteau JE, Brubakk AO, Gempp E, Castagna O, Risso JJ, Vallée N. Sidenafil pre-treatment promotes decompression sickness in rats. PLoS One. 2013. 8(4):e60639. [Medline]. [Full Text].
Taylor LH. A Diver's Guide To Nitrogen Species. University of Michigan. Available at http://www-personal.umich.edu/~lpt/nitrogen.htm. Accessed: April 1, 2014.
Thom SR, Milovanova TN, Bogush M, Yang M, Bhopale VM, Pollock NW, et al. Bubbles, microparticles, and neutrophil activation: changes with exercise level and breathing gas during open-water SCUBA diving. J Appl Physiol (1985). 2013 May 15. 114(10):1396-405. [Medline].
Boussuges A, Succo E, Juhan-Vague I, Sainty JM. Activation of coagulation in decompression illness. Aviat Space Environ Med. 1998 Feb. 69(2):129-32. [Medline].
Oode Y, Yanagawa Y, Inoue T, Oomori K, Osaka H, Okamoto K. Cutaneous manifestation of decompression sickness: cutis marmorata. Intern Med. 2013. 52(21):2479. [Medline].
Kemper TC, Rienks R, van Ooij PJ, van Hulst RA. Cutis marmorata in decompression illness may be cerebrally mediated: a novel hypothesis on the aetiology of cutis marmorata. Diving Hyperb Med. 2015 Jun. 45 (2):84-8. [Medline].
Wilmshurst PT. Cutis marmorata and cerebral arterial gas embolism. Diving Hyperb Med. 2015 Dec. 45 (4):261. [Medline].
Germonpre P, Balestra C, Obeid G, Caers D. Cutis Marmorata skin decompression sickness is a manifestation of brainstem bubble embolization, not of local skin bubbles. Med Hypotheses. 2015 Dec. 85 (6):863-9. [Medline].
Xu W, Liu W, Huang G, Zou Z, Cai Z, Xu W. Decompression illness: clinical aspects of 5278 consecutive cases treated in a single hyperbaric unit. PLoS One. 2012. 7(11):e50079. [Medline]. [Full Text].
Hennedige T, Chow W, Ng YY, Chung-Tsing GC, Lim TC, Kei PL. MRI in spinal cord decompression sickness. J Med Imaging Radiat Oncol. 2012 Jun. 56(3):282-8. [Medline].
Gempp E, Blatteau JE, Stephant E, Pontier JM, Constantin P, Pény C. MRI findings and clinical outcome in 45 divers with spinal cord decompression sickness. Aviat Space Environ Med. 2008 Dec. 79(12):1112-6. [Medline].
Blatteau JE, Gempp E, Simon O, Coulange M, Delafosse B, Souday V, et al. Prognostic factors of spinal cord decompression sickness in recreational diving: retrospective and multicentric analysis of 279 cases. Neurocrit Care. 2011 Aug. 15(1):120-7. [Medline].
Mathew B, Laden G. Management of severe spinal cord injury following hyperbaric exposure. Diving Hyperb Med. 2015 Sep. 45 (3):210. [Medline].
Schipke JD, Tetzlaff K. Why predominantly neurological decompression sickness in breath-hold divers?. J Appl Physiol (1985). 2016 Jun 15. 120 (12):1474-7. [Medline].
James PB. Hyperbaric oxygenation in fluid microembolism. Neurol Res. 2007 Mar. 29(2):156-61. [Medline].
Latham E, van Hoesen K, Grover I. Diplopia due to mask barotrauma. J Emerg Med. 2008 Nov 6. [Medline].
Uzun C, Yagiz R, Tas A, Adali MK, Inan N, Koten M, et al. Alternobaric vertigo in sport SCUBA divers and the risk factors. J Laryngol Otol. 2003 Nov. 117(11):854-60. [Medline].
Klingmann C, Benton PJ, Ringleb PA, Knauth M. Embolic inner ear decompression illness: correlation with a right-to-left shunt. Laryngoscope. 2003 Aug. 113(8):1356-61. [Medline].
Klingmann C, Praetorius M, Baumann I, Plinkert PK. Barotrauma and decompression illness of the inner ear: 46 cases during treatment and follow-up. Otol Neurotol. 2007 Jun. 28(4):447-54. [Medline].
Klingmann C. Inner ear decompression sickness in compressed-air diving. Undersea Hyperb Med. 2012 Jan-Feb. 39(1):589-94. [Medline].
Gempp E, Louge P. Inner ear decompression sickness in scuba divers: a review of 115 cases. Eur Arch Otorhinolaryngol. 2013 May. 270(6):1831-7. [Medline].
Goplen FK, Grønning M, Irgens A, Sundal E, Nordahl SH. Vestibular symptoms and otoneurological findings in retired offshore divers. Aviat Space Environ Med. 2007 Apr. 78(4):414-9. [Medline].
Mitchell SJ, Doolette DJ. Selective vulnerability of the inner ear to decompression sickness in divers with right-to-left shunt: the role of tissue gas supersaturation. J Appl Physiol. 2009 Jan. 106(1):298-301. [Medline].
Ignatescu M, Bryson P, Klingmann C. Susceptibility of the inner ear structure to shunt-related decompression sickness. Aviat Space Environ Med. 2012 Dec. 83(12):1145-51. [Medline].
Tremolizzo L, Malpieri M, Ferrarese C, Appollonio I. Inner-ear decompression sickness: 'hubble-bubble' without brain trouble?. Diving Hyperb Med. 2015 Jun. 45 (2):135-6. [Medline].
Mitchell SJ, Doolette DJ. Pathophysiology of inner ear decompression sickness: potential role of the persistent foramen ovale. Diving Hyperb Med. 2015 Jun. 45 (2):105-10. [Medline].
Lampert R. Evaluation and management of arrhythmia in the athletic patient. Prog Cardiovasc Dis. 2012 Mar-Apr. 54(5):423-31. [Medline].
Mukundakrishnan K, Ayyaswamy PS, Eckmann DM. Computational simulation of hematocrit effects on arterial gas embolism dynamics. Aviat Space Environ Med. 2012 Feb. 83(2):92-101. [Medline]. [Full Text].
Williams ST, Prior FG, Bryson P. Hematocrit change in tropical scuba divers. Wilderness Environ Med. 2007. 18(1):48-53. [Medline].
Newton HB, Burkart J, Pearl D, Padilla W. Neurological decompression illness and hematocrit: analysis of a consecutive series of 200 recreational scuba divers. Undersea Hyperb Med. 2008 Mar-Apr. 35(2):99-106. [Medline].
Fahlman A, Dromsky DM. Dehydration effects on the risk of severe decompression sickness in a swine model. Aviat Space Environ Med. 2006 Feb. 77(2):102-6. [Medline].
Gempp E, Blatteau JE, Pontier JM, Balestra C, Louge P. Preventive effect of pre-dive hydration on bubble formation in divers. Br J Sports Med. 2009 Mar. 43(3):224-8. [Medline].
Hjelde A, Bergh K, Brubakk AO, Iversen OJ. Complement activation in divers after repeated air/heliox dives and its possible relevance to DCS. J Appl Physiol. 1995 Mar. 78(3):1140-4. [Medline].
Huang KL, Lin YC. Activation of complement and neutrophils increases vascular permeability during air embolism. Aviat Space Environ Med. 1997 Apr. 68(4):300-5. [Medline].
Shastri KA, Logue GL, Lundgren CE, Logue CJ, Suggs DF. Diving decompression fails to activate complement. Undersea Hyperb Med. 1997 Jun. 24(2):51-7. [Medline].
Koch AE, Kirsch H, Reuter M, Warninghoff V, Rieckert H, Deuschl G. Prevalence of patent foramen ovale (PFO) and MRI-lesions in mild neurological decompression sickness (type B-DCS/AGE). Undersea Hyperb Med. 2008 May-Jun. 35(3):197-205. [Medline].
Koch AE, Wegner-Bröse H, Warninghoff V, Deuschl G. Viewpoint: the type A- and the type B-variants of Decompression Sickness. Undersea Hyperb Med. 2008 Mar-Apr. 35(2):91-7. [Medline].
Bove AA. Risk of decompression sickness with patent foramen ovale. Undersea Hyperb Med. 1998. 25(3):175-8. [Medline].
Germonpre P, Dendale P, Unger P, Balestra C. Patent foramen ovale and decompression sickness in sports divers. J Appl Physiol. 1998 May. 84(5):1622-6. [Medline].
Wilmshurst PT, Morrison WL, Walsh KP. Comparison of the size of persistent foramen ovale and atrial septal defects in divers with shunt-related decompression illness and in the general population. Diving Hyperb Med. 2015 Jun. 45 (2):89-93. [Medline].
Germonpré P. Persistent (patent) foramen ovale (PFO): implications for safe diving. Diving Hyperb Med. 2015 Jun. 45 (2):73-4. [Medline].
Aslam F, Shirani J, Haque AA. Patent foramen ovale: assessment, clinical significance and therapeutic options. South Med J. 2006 Dec. 99(12):1367-72. [Medline].
Drighil A, El Mosalami H, Elbadaoui N, Chraibi S, Bennis A. Patent foramen ovale: a new disease?. Int J Cardiol. 2007 Oct 31. 122(1):1-9. [Medline].
Harrah JD, O'Boyle PS, Piantadosi CA. Underutilization of echocardiography for patent foramen ovale in divers with serious decompression sickness. Undersea Hyperb Med. 2008 May-Jun. 35(3):207-11. [Medline].
Honěk J, Šefc L, Honěk T, Šrámek M, Horváth M, Veselka J. Patent Foramen Ovale in Recreational and Professional Divers: An Important and Largely Unrecognized Problem. Can J Cardiol. 2015 Aug. 31 (8):1061-6. [Medline].
Cartoni D, De Castro S, Valente G, Costanzo C, Pelliccia A, Beni S, et al. Identification of professional scuba divers with patent foramen ovale at risk for decompression illness. Am J Cardiol. 2004 Jul 15. 94(2):270-3. [Medline].
Trevett AJ, Sheehan C, Forbes R. Decompression illness presenting as breast pain. Undersea Hyperb Med. 2006 Mar-Apr. 33(2):77-9. [Medline].
Honek T, Veselka J, Tomek A, Srámek M, Janugka J, Sefc L, et al. [Paradoxical embolization and patent foramen ovale in scuba divers: screening possibilities]. Vnitr Lek. 2007 Feb. 53(2):143-6. [Medline].
Rasmussen W. Saline Shunt Study for the Evaluation of an ASD or PFO. Imaging Skills for Echocardiography. Available at http://echocardiographyskills.com/saline-shunt-study-asd-and-pfo. Accessed: June 30, 2016.
Beda RD, Gill EA Jr. Patent foramen ovale: does it play a role in the pathophysiology of migraine headache?. Cardiol Clin. 2005 Feb. 23(1):91-6. [Medline].
Wilmshurst PT, Nightingale S, Walsh KP, Morrison WL. Effect on migraine of closure of cardiac right-to-left shunts to prevent recurrence of decompression illness or stroke or for haemodynamic reasons. Lancet. 2000 Nov 11. 356(9242):1648-51. [Medline].
Sastry S, MacNab A, Daly K, Ray S, McCollum C. Transcranial Doppler detection of venous-to-arterial circulation shunts: criteria for patent foramen ovale. J Clin Ultrasound. 2009 Jun. 37(5):276-80. [Medline].
Honek J, Honek T, Januška J, Sebesta P, Novotný S, Sefc L, et al. [Patent foramen ovale and the risk of paradoxical embolization of venous bubbles in divers - cave for foam sclerotization of varicose veins]. Rozhl Chir. 2012 Jul. 91(7):378-80. [Medline].
Billinger M, Zbinden R, Mordasini R, Windecker S, Schwerzmann M, Meier B, et al. Patent foramen ovale closure in recreational divers: effect on decompression illness and ischaemic brain lesions during long-term follow-up. Heart. 2011 Dec. 97(23):1932-7. [Medline].
Leffler CT, White JC. Recompression treatments during the recovery of TWA Flight 800. Undersea Hyperb Med. 1997 Winter. 24(4):301-8. [Medline].
Schultz GJ. Accusations "reckless and a mistake," says co-author. America's NAVY. Available at http://www.navy.mil/navydata/nav_legacy.asp?id=284. 2009 Sep 16; Accessed: June 30, 2016.
Huang KL, Wu CP, Chen YL, Kang BH, Lin YC. Heat stress attenuates air bubble-induced acute lung injury: a novel mechanism of diving acclimatization. J Appl Physiol. 2003 Apr. 94(4):1485-90. [Medline].
Su CL, Wu CP, Chen SY, Kang BH, Huang KL, Lin YC. Acclimatization to neurological decompression sickness in rabbits. Am J Physiol Regul Integr Comp Physiol. 2004 Nov. 287(5):R1214-8. [Medline].
Chen Y, Montcalm-Smith E, Schlaerth C, Auker C, McCarron RM. Acclimation to decompression: stress and cytokine gene expression in rat lungs. J Appl Physiol (1985). 2011 Oct. 111(4):1007-13. [Medline].
Sporting Goods Manufacturers Association. Sports Participation in America Topline Report 2004. August 2004. Available at http://sgma.affiniscape.com/associations/5119/files/sport-part-topline2004.pdf.
Sporting Goods Manufacturers Association. Sports Participation in America 2004. August 2004. Available at http://www.sgma.com/associations/5119/files/p27-02-04-m.pdf.
Sporting Goods Manufacturers Association. 2007 Sports and Fitness Participation Report. 2007. Available at http://www.sgma.com/associations/5119/files/topline07.pdf.
The Sports & Fitness Industry Association. Scuba Diving Participation Report 2013. SFIA. Available at http://www.sfia.org/reports/84_Scuba-Diving-Participation-Report-2013. Accessed: March 17, 2014.
Glazer TA, Telian SA. Otologic Hazards Related to Scuba Diving. Sports Health. 2016 Feb 8. [Medline].
Lee YI, Ye BJ. Underwater and hyperbaric medicine as a branch of occupational and environmental medicine. Ann Occup Environ Med. 2013 Dec 19. 25(1):39. [Medline]. [Full Text].
van der Hulst GA, Buzzacott PL. Diver Health Survey score and probability of decompression sickness among occupational dive guides and instructors. Diving Hyperb Med. 2012 Mar. 42(1):18-23. [Medline].
Gempp E, Blatteau JE. Preconditioning methods and mechanisms for preventing the risk of decompression sickness in scuba divers: a review. Res Sports Med. 2010 Jul. 18(3):205-18. [Medline].
United States of America. Health Insurance Portability and Accountability Act of 1996. Health Information Privacy. Available at http://www.hhs.gov/ocr/privacy/hipaa/understanding/index.html. Accessed: March 17, 2014.
Bennett PB. What me bent?. Alert Diver (Divers Alert Network). 1997. Vol 2:
Taylor DM, O'Toole KS, Ryan CM. Experienced, recreational scuba divers in Australia continue to dive despite medical contraindications. Wilderness Environ Med. 2002. 13(3):187-93. [Medline].
St Leger Dowse M, Waterman MK, Penny CE, Smerdon GR. Does self-certification reflect the cardiac health of UK sport divers?. Diving Hyperb Med. 2015 Sep. 45 (3):184-9. [Medline].
Divers Alert Network. Report on Decompression Illness, DivingFatalities and Project Dive Exploration 2005 Edition. 2005. Available at http://dan.org/medical/report/2005DCIReport.pdf.
Divers Alert Network. Annual Diving Report 2006 Edition. Oct 11, 2006. Available at http://dan.org/medical/report/2006DANDivingReport.pdf.
Goldhahn RT Jr. Scuba diving deaths: a review and approach for the pathologist. Leg Med Annu. 1977. 1976:109-32. [Medline].
Lewis PR. Skin diving fatalities in New Zealand. N Z Med J. 1979 Jun 27. 89(638):472-5. [Medline].
Arness MK. Scuba decompression illness and diving fatalities in an overseas military community. Aviat Space Environ Med. 1997 Apr. 68(4):325-33. [Medline].
Klingmann C, Gonnermann A, Dreyhaupt J, Vent J, Praetorius M, Plinkert PK. Decompression illness reported in a survey of 429 recreational divers. Aviat Space Environ Med. 2008 Feb. 79(2):123-8. [Medline].
Eichhorn L, Leyk D. Diving medicine in clinical practice. Dtsch Arztebl Int. 2015 Feb 27. 112 (9):147-57; quiz 158. [Medline].
Landsberg PG. South African underwater diving accidents, 1969-1976. S Afr Med J. 1976 Dec 25. 50(55):2155-59. [Medline].
Denoble PJ, Caruso JL, Dear Gde L, Pieper CF, Vann RD. Common causes of open-circuit recreational diving fatalities. Undersea Hyperb Med. 2008 Nov-Dec. 35(6):393-406. [Medline].
Tomassoni AJ. Cardiac problems associated with dysbarism. Cardiol Clin. 1995 May. 13(2):266-71. [Medline].
Cialoni D, Pieri M, Balestra C, Marroni A. Flying after diving: should recommendations be reviewed? In-flight echocardiographic study in bubble-prone and bubble-resistant divers. Diving Hyperb Med. 2015 Mar. 45 (1):10-5. [Medline].
Buch DA, El Moalem H, Dovenbarger JA, Uguccioni DM, Moon RE. Cigarette smoking and decompression illness severity: a retrospective study in recreational divers. Aviat Space Environ Med. 2003 Dec. 74(12):1271-4. [Medline].
Morgan WP, Raglin JS, O'Connor PJ. Trait anxiety predicts panic behavior in beginning scuba students. Int J Sports Med. 2004 May. 25(4):314-22. [Medline].
Schellart NA, van Rees Vellinga TP, van Hulst RA. Body fat does not affect venous bubble formation after air dives of moderate severity: theory and experiment. J Appl Physiol (1985). 2013 Mar 1. 114(5):602-10. [Medline].
Schellart NA, Vellinga TP, van Dijk FJ, Sterk W. Doppler bubble grades after diving and relevance of body fat. Aviat Space Environ Med. 2012 Oct. 83(10):951-7. [Medline].
Kaczerska D, Pleskacz K, Siermontowski P, Olszański R, Krefft K. Risk factors increasing health hazards after air dives. Undersea Hyperb Med. 2015 Nov-Dec. 42 (6):565-72. [Medline].
Pollock NW. Re: Don't dive cold when you don't have to. Diving Hyperb Med. 2015 Sep. 45 (3):209. [Medline].
Gerth WA. On diver thermal status and susceptibility to decompression sickness. Diving Hyperb Med. 2015 Sep. 45 (3):208. [Medline].
Reuter M, Tetzlaff K, Hutzelmann A, Fritsch G, Steffens JC, Bettinghausen E, et al. MR imaging of the central nervous system in diving-related decompression illness. Acta Radiol. 1997 Nov. 38(6):940-4. [Medline].
Sparacia G, Banco A, Sparacia B, Midiri M, Brancatelli G, Accardi M, et al. Magnetic resonance findings in scuba diving-related spinal cord decompression sickness. MAGMA. 1997 Jun. 5(2):111-5. [Medline].
McCormac J, Mirvis SE, Cotta-Cumba C, Shanmuganathan K. Spinal myelopathy resulting from decompression sickness: MR findings in a case and review of the literature. Emerg Radiol. 2002 Oct. 9(4):240-2. [Medline].
Blogg SL, Loveman GA, Seddon FM, Woodger N, Koch A, Reuter M, et al. Magnetic resonance imaging and neuropathology findings in the goat nervous system following hyperbaric exposures. Eur Neurol. 2004. 52(1):18-28. [Medline].
Gao GK, Wu D, Yang Y, Yu T, Xue J, Wang X, et al. Cerebral magnetic resonance imaging of compressed air divers in diving accidents. Undersea Hyperb Med. 2009 Jan-Feb. 36(1):33-41. [Medline].
Aksoy FG. MR imaging of subclinical cerebral decompression sickness. A case report. Acta Radiol. 2003 Jan. 44(1):108-10. [Medline].
Yoshiyama M, Asamoto S, Kobayashi N, Sugiyama H, Doi H, Sakagawa H, et al. Spinal cord decompression sickness associated with scuba diving: correlation of immediate and delayed magnetic resonance imaging findings with severity of neurologic impairment--a report on 3 cases. Surg Neurol. 2007 Mar. 67(3):283-7. [Medline].
Tetzlaff K, Friege L, Hutzelmann A, Reuter M, Holl D, Leplow B. Magnetic resonance signal abnormalities and neuropsychological deficits in elderly compressed-air divers. Eur Neurol. 1999. 42(4):194-9. [Medline].
Hutchinson EB, Sobakin AS, Meyerand ME, Eldridge M, Ferrazzano P. Diffusion tensor MRI of spinal decompression sickness. Undersea Hyperb Med. 2013 Jan-Feb. 40(1):23-31. [Medline]. [Full Text].
Pierce NE, Parell GJ, Jesus RO, Ojano-Dirain CP, Antonelli PJ. Magnetic resonance imaging in a guinea pig model of inner ear decompression sickness and barotrauma. Laryngoscope. 2015 Dec 9. [Medline].
Blatteau JE, Jean F, Pontier JM, Blanche E, Bompar JM, Meaudre E. [Decompression sickness accident management in remote areas. Use of immediate in-water recompression therapy. Review and elaboration of a new protocol targeted for a mission at Clipperton atoll]. Ann Fr Anesth Reanim. 2006 Aug. 25(8):874-83. [Medline].
Gold D, Aiyarak S, Wongcharoenyong S, Geater A, Juengprasert W, Gerth WA. The indigenous fisherman divers of Thailand: diving practices. Int J Occup Saf Ergon. 2000. 6(1):89-112. [Medline].
Gold D, Geater A, Aiyarak S, Juengprasert W, Chuchaisangrat B, Samakkaran A. The indigenous fisherman divers of Thailand: in-water recompression. Int Marit Health. 1999. 50(1-4):39-48. [Medline].
Gold D, Geater A, Aiyarak S, Wongcharoenyong S, Juengprasert W, Johnson M, et al. The indigenous fisherman divers of Thailand: diving-related mortality and morbidity. Int J Occup Saf Ergon. 2000. 6(2):147-67. [Medline].
Blatteau JE, Pontier JM, Buzzacott P, Lambrechts K, Nguyen VM, Cavenel P, et al. Prevention and treatment of decompression sickness using training and in-water recompression among fisherman divers in Vietnam. Inj Prev. 2016 Feb. 22 (1):25-32. [Medline].
Longphre JM, Denoble PJ, Moon RE, Vann RD, Freiberger JJ. First aid normobaric oxygen for the treatment of recreational diving injuries. Undersea Hyperb Med. 2007 Jan-Feb. 34(1):43-9. [Medline].
Bessereau J, Coulange M, Genotelle N, Barthélémy A, Michelet P, Bruguerolle B, et al. [Aspirin in decompression sickness]. Therapie. 2008 Nov-Dec. 63(6):419-23. [Medline].
Bessereau J, Genotelle N, Brun PM, Aboab J, Antona M, Chenaitia H, et al. Decompression sickness in urban divers in France. Int Marit Health. 2012. 63(3):170-3. [Medline].
Westerweel PE, Fijen VA, Van Hulst RA. Aspirin in the treatment of decompression sickness: what can we learn from French experience?. Int Marit Health. 2013. 64(1):51. [Medline].
Bessereau J, Annane D. Response to letter to the editor by Westerweel et al., entitled 'aspirin in the treatment of decompression sickness: what can we learn from French experience?' [Int Marit Health 2013; 64, 1: 51]. Int Marit Health. 2013. 64(3):175. [Medline].
Bennett MH, Lehm JP, Mitchell SJ, Wasiak J. Recompression and adjunctive therapy for decompression illness. Cochrane Database Syst Rev. 2012 May 16. 5:CD005277. [Medline].
de Watteville G. [A critical assessment of Trendelenburg's position in the acute phase after a diving accident]. Schweiz Z Sportmed. 1993 Sep. 41(3):123-5. [Medline].
Chin W, Jacoby L, Simon O, Talati N, Wegrzyn G, Jacoby R, et al. Hyperbaric programs in the United States: Locations and capabilities of treating decompression sickness, arterial gas embolisms, and acute carbon monoxide poisoning: survey results. Undersea Hyperb Med. 2016 Jan-Feb. 43 (1):29-43. [Medline].
Goldenberg I, Shupak A, Shoshani O. Oxy-helium treatment for refractory neurological decompression sickness: a case report. Aviat Space Environ Med. 1996 Jan. 67(1):57-60. [Medline].
Shupak A, Melamed Y, Ramon Y, Bentur Y, Abramovich A, Kol S. Helium and oxygen treatment of severe air-diving-induced neurologic decompression sickness. Arch Neurol. 1997 Mar. 54(3):305-11. [Medline].
Tempel R, Severance HW. Proposing short-term observation units for the management of decompression illness. Undersea Hyperb Med. 2006 Mar-Apr. 33(2):89-94. [Medline].
Kot J, Sicko Z, Michalkiewicz M, Lizak E, Góralczyk P. Recompression treatment for decompression illness: 5-year report (2003-2007) from National Centre for Hyperbaric Medicine in Poland. Int Marit Health. 2008. 59(1-4):69-80. [Medline].
Gil A, Shupak A, Lavon H, Adir Y. [Decompression sickness in divers treated at the Israel Naval Medical Institute between the years 1992 to 1997]. Harefuah. 2000 May 1. 138(9):751-4, 806. [Medline].
Blatteau JE, Gempp E, Constantin P, Louge P. Risk factors and clinical outcome in military divers with neurological decompression sickness: influence of time to recompression. Diving Hyperb Med. 2011 Sep. 41(3):129-34. [Medline].
Mutzbauer TS, Staps E. How delay to recompression influences treatment and outcome in recreational divers with mild to moderate neurological decompression sickness in a remote setting. Diving Hyperb Med. 2013 Mar. 43(1):42-5. [Medline].
Hadanny A, Fishlev G, Bechor Y, Bergan J, Friedman M, Maliar A, et al. Delayed recompression for decompression sickness: retrospective analysis. PLoS One. 2015. 10 (4):e0124919. [Medline].
Dromsky DM, Spiess BD, Fahlman A. Treatment of decompression sickness in swine with intravenous perfluorocarbon emulsion. Aviat Space Environ Med. 2004 Apr. 75(4):301-5. [Medline].
Zhu J, Hullett JB, Somera L, Barbee RW, Ward KR, Berger BE, et al. Intravenous perfluorocarbon emulsion increases nitrogen washout after venous gas emboli in rabbits. Undersea Hyperb Med. 2007 Jan-Feb. 34(1):7-20. [Medline].
Spahn DR. Blood substitutes. Artificial oxygen carriers: perfluorocarbon emulsions. Crit Care. 1999. 3(5):R93-7. [Medline]. [Full Text].
Smith CR, Parsons JT, Zhu J, Spiess BD. The effect of intravenous perfluorocarbon emulsions on whole-body oxygenation after severe decompression sickness. Diving Hyperb Med. 2012 Mar. 42(1):10-7. [Medline].
Zhang RJ, Liu K, Kang ZM, Fan DF, Ni XX, Liu Y, et al. Combined effects of intravenous perfluorocarbon emulsion and oxygen breathing on decompression-induced spinal cord injury in rats. Undersea Hyperb Med. 2011 Sep-Oct. 38(5):335-43. [Medline].
Mahon RT, Auker CR, Bradley SG, Mendelson A, Hall AA. The emulsified perfluorocarbon Oxycyte improves spinal cord injury in a swine model of decompression sickness. Spinal Cord. 2013 Mar. 51(3):188-92. [Medline].
Spiess BD. Perfluorocarbon emulsions as a promising technology: a review of tissue and vascular gas dynamics. J Appl Physiol. 2009 Apr. 106(4):1444-52. [Medline].
Spiess BD, Zhu J, Pierce B, Weis R, Berger BE, Reses J, et al. Effects of perfluorocarbon infusion in an anesthetized swine decompression model. J Surg Res. 2009 May 1. 153(1):83-94. [Medline].
Cronin WA, Senese AL, Arnaud FG, Regis DP, Auker CR, Mahon RT. The effect of the perfluorocarbon emulsion Oxycyte on platelet count and function in the treatment of decompression sickness in a swine model. Blood Coagul Fibrinolysis. 2015 Dec 8. [Medline].
Dainer H, Nelson J, Brass K, Montcalm-Smith E, Mahon R. Short oxygen prebreathing and intravenous perfluorocarbon emulsion reduces morbidity and mortality in a swine saturation model of decompression sickness. J Appl Physiol. 2007 Mar. 102(3):1099-104. [Medline].
Cianci P, Slade JB Jr. Delayed treatment of decompression sickness with short, no-air-break tables: review of 140 cases. Aviat Space Environ Med. 2006 Oct. 77(10):1003-8. [Medline].
Weisher DD. Resolution of neurological DCI after long treatment delays. Undersea Hyperb Med. 2008 May-Jun. 35(3):159-61. [Medline].
Dunford RG, Vann RD, Gerth WA, Pieper CF, Huggins K, Wacholtz C, et al. The incidence of venous gas emboli in recreational diving. Undersea Hyperb Med. 2002. 29(4):247-59. [Medline].
Barratt DM, Van Meter K. Decompression sickness in Miskito Indian lobster divers: review of 229 cases. Aviat Space Environ Med. 2004 Apr. 75(4):350-3. [Medline].
MacDonald RD, O'Donnell C, Allan GM, Breeck K, Chow Y, DeMajo W. Interfacility transport of patients with decompression illness: literature review and consensus statement. Prehosp Emerg Care. 2006 Oct-Dec. 10(4):482-7. [Medline].
Bennett PB. Putting on the brakes: extra safety stops and slower ascent rates may help reduce decompression injuries. Alert Diver (Divers Alert Network). 2001. 1.
Bennett PB, Marroni A, Cronje FJ, Cali-Corleo R, Germonpre P, Pieri M, et al. Effect of varying deep stop times and shallow stop times on precordial bubbles after dives to 25 msw (82 fsw). Undersea Hyperb Med. 2007 Nov-Dec. 34(6):399-406. [Medline].
Blatteau JE, Hugon J, Gempp E, Castagna O, Pény C, Vallée N. Oxygen breathing or recompression during decompression from nitrox dives with a rebreather: effects on intravascular bubble burden and ramifications for decompression profiles. Eur J Appl Physiol. 2012 Jun. 112(6):2257-65. [Medline].
Jankowski LW, Tikuisis P, Nishi RY. Exercise effects during diving and decompression on postdive venous gas emboli. Aviat Space Environ Med. 2004 Jun. 75(6):489-95. [Medline].
Dujic Z, Valic Z, Brubakk AO. Beneficial role of exercise on scuba diving. Exerc Sport Sci Rev. 2008 Jan. 36(1):38-42. [Medline].
Dujic Z, Palada I, Obad A, Duplancic D, Bakovic D, Valic Z. Exercise during a 3-min decompression stop reduces postdive venous gas bubbles. Med Sci Sports Exerc. 2005 Aug. 37(8):1319-23. [Medline].
O'Connor PE. The nontechnical causes of diving accidents: can U.S. Navy divers learn from other industries?. Undersea Hyperb Med. 2007 Jan-Feb. 34(1):51-9. [Medline].
Gutvik CR, Brubakk AO. A dynamic two-phase model for vascular bubble formation during decompression of divers. IEEE Trans Biomed Eng. 2009 Mar. 56(3):884-9. [Medline].
Mollerlokken A, Berge VJ, Jorgensen A, Wisloff U, Brubakk AO. Effect of a short-acting NO donor on bubble formation from a saturation dive in pigs. J Appl Physiol. 2006 Dec. 101(6):1541-5. [Medline].
Dujic Z, Palada I, Valic Z, Duplancic D, Obad A, Wisløff U. Exogenous nitric oxide and bubble formation in divers. Med Sci Sports Exerc. 2006 Aug. 38(8):1432-5. [Medline].
Madden LA, Laden G. Gas bubbles may not be the underlying cause of decompression illness - The at-depth endothelial dysfunction hypothesis. Med Hypotheses. 2009 Apr. 72(4):389-92. [Medline].
Blatteau JE, Barre S, Pascual A, Castagna O, Abraini JH, Risso JJ, et al. Protective effects of fluoxetine on decompression sickness in mice. PLoS One. 2012. 7(11):e49069. [Medline]. [Full Text].
Blatteau JE, de Maistre S, Lambrechts K, Abraini J, Risso JJ, Vallée N. Fluoxetine stimulates anti-inflammatory IL-10 cytokine production and attenuates sensory deficits in a rat model of decompression sickness. J Appl Physiol (1985). 2015 Dec 15. 119 (12):1393-9. [Medline].
Zhang K, Wang D, Xu J, Li R, Cai Z, Liu K, et al. Simvastatin decreases incidence of decompression sickness in rats. Undersea Hyperb Med. 2015 Mar-Apr. 42 (2):115-23. [Medline].
Dujic Z, Obad A, Palada I, Ivancev V, Valic Z. Venous bubble count declines during strenuous exercise after an open sea dive to 30 m. Aviat Space Environ Med. 2006 Jun. 77(6):592-6. [Medline].
Wisløff U, Brubakk AO. Aerobic endurance training reduces bubble formation and increases survival inrats exposed to hyperbaric pressure. J Physiol. 2001 Dec 1. 537(Pt 2):607-11. [Medline].
Dujic Z, Duplancic D, Marinovic-Terzic I, Bakovic D, Ivancev V, Valic Z, et al. Aerobic exercise before diving reduces venous gas bubble formation in humans. J Physiol. 2004 Mar 16. 555(Pt 3):637-42. [Medline].
Loset A Jr, Mollerlokken A, Berge V, Wisloff U, Brubakk AO. Post-dive bubble formation in rats: effects of exercise 24 h ahead repeated 30min before the dive. Aviat Space Environ Med. 2006 Sep. 77(9):905-8. [Medline].
Berge VJ, Jørgensen A, Løset A, Wisløff U, Brubakk AO. Exercise ending 30 min pre-dive has no effect on bubble formation in the rat. Aviat Space Environ Med. 2005 Apr. 76(4):326-8. [Medline].
Blatteau JE, Boussuges A, Gempp E, Pontier JM, Castagna O, Robinet C, et al. Haemodynamic changes induced by submaximal exercise before a dive and its consequences on bubble formation. Br J Sports Med. 2007 Jun. 41(6):375-9. [Medline].
Pendergast DR, Senf C, Lundgren CE. Is the rate of whole-body nitrogen elimination influenced by exercise?. Undersea Hyperb Med. 2012 Jan-Feb. 39(1):595-604. [Medline].
Gennser M, Jurd KM, Blogg SL. Pre-dive exercise and post-dive evolution of venous gas emboli. Aviat Space Environ Med. 2012 Jan. 83(1):30-4. [Medline].
Wisløff U, Richardson RS, Brubakk AO. Exercise and nitric oxide prevent bubble formation: a novel approach to the prevention of decompression sickness?. J Physiol. 2004 Mar 16. 555:825-9. [Medline].
Wisløff U, Richardson RS, Brubakk AO. NOS inhibition increases bubble formation and reduces survival in sedentary but not exercised rats. J Physiol. 2003 Jan 15. 546:577-82. [Medline].
Pontier JM, Guerrero F, Castagna O. Bubble formation and endothelial function before and after 3 months of dive training. Aviat Space Environ Med. 2009 Jan. 80(1):15-9. [Medline].
Madden D, Thom SR, Dujic Z. Exercise before and after SCUBA diving and the role of cellular microparticles in decompression stress. Med Hypotheses. 2016 Jan. 86:80-4. [Medline].
Castagna O, Gempp E, Blatteau JE. Pre-dive normobaric oxygen reduces bubble formation in scuba divers. Eur J Appl Physiol. 2009 May. 106(2):167-72. [Medline].
Mahon RT, Dainer HM, Gibellato MG, Soutiere SE. Short oxygen prebreathe periods reduce or prevent severe decompression sickness in a 70-kg swine saturation model. J Appl Physiol. 2009 Apr. 106(4):1459-63. [Medline].
Sobakin AS, Wilson MA, Lehner CE, Dueland RT, Gendron-Fitzpatrick AP. Oxygen pre-breathing decreases dysbaric diseases in UW sheep undergoing hyperbaric exposure. Undersea Hyperb Med. 2008 Jan-Feb. 35(1):61-7. [Medline].
Wang FF, Fang YQ, You P, Bao XC, Ma J, Zhang S. [Effect of different pressure oxygen pre-breathe in diving decompression sickness of rats]. Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2015 Sep. 31 (5):401-4. [Medline].
Blatteau JE, Gempp E, Balestra C, Mets T, Germonpre P. Predive sauna and venous gas bubbles upon decompression from 400 kPa. Aviat Space Environ Med. 2008 Dec. 79(12):1100-5. [Medline].
Fismen L, Hjelde A, Svardal AM, Djurhuus R. Differential effects on nitric oxide synthase, heat shock proteins and glutathione in human endothelial cells exposed to heat stress and simulated diving. Eur J Appl Physiol. 2012 Jul. 112(7):2717-25. [Medline].
Ni XX, Ni M, Fan DF, Sun Q, Kang ZM, Cai ZY, et al. Heat-shock protein 70 is involved in hyperbaric oxygen preconditioning on decompression sickness in rats. Exp Biol Med (Maywood). 2013 Jan. 238(1):12-22. [Medline].
Candito M, Candito E, Chatel M, van Obberghen E, Dunac A. [Homocysteinemia and thrombophilic factors in unexplained decompression sickness]. Rev Neurol (Paris). 2006 Sep. 162(8-9):840-4. [Medline].
Candito M, Chatel M, Candito E, Lapoussiere M, Mengual R, Van Obberghen E, et al. [Thrombophilic factors in divers with undeserved decompression sickness]. Pathol Biol (Paris). 2006 Apr. 54(3):155-8. [Medline].
Eftedal OS, Lydersen S, Brubakk AO. The relationship between venous gas bubbles and adverse effects of decompression after air dives. Undersea Hyperb Med. 2007 Mar-Apr. 34(2):99-105. [Medline].
Tufan K, Ademoglu A, Kurtaran E, Yildiz G, Aydin S, Egi SM. Automatic detection of bubbles in the subclavian vein using Doppler ultrasound signals. Aviat Space Environ Med. 2006 Sep. 77(9):957-62. [Medline].
Ball R, Schwartz SL. Kinetic and dynamic models of diving gases in decompression sickness prevention. Clin Pharmacokinet. 2002. 41(6):389-402. [Medline].
Brubakk AO, Arntzen AJ, Wienke BR, Koteng S. Decompression profile and bubble formation after dives with surface decompression: experimental support for a dual phase model of decompression. Undersea Hyperb Med. 2003. 30(3):181-93. [Medline].
Montcalm-Smith E, Caviness J, Chen Y, McCarron RM. Stress biomarkers in a rat model of decompression sickness. Aviat Space Environ Med. 2007 Feb. 78(2):87-93. [Medline].
Lemeshchenko GP, Isaeva NM. [A toxicological evaluation of micromycetes isolated from salmon roe]. Mikrobiol Zh. 1990 Mar-Apr. 52(2):66-9. [Medline].
Kondo Y, Shiohira S, Kamizato K, Teruya K, Fuchigami T, Kakinohana M, et al. Vascular hyperpermeability in pulmonary decompression illness: 'the chokes'. Emerg Med Australas. 2012 Aug. 24(4):460-2. [Medline].
Gempp E, Morin J, Louge P, Blatteau JE. Reliability of plasma D-dimers for predicting severe neurological decompression sickness in scuba divers. Aviat Space Environ Med. 2012 Aug. 83(8):771-5. [Medline].
Blatteau JE, David HN, Vallée N, Meckler C, Demaistre S, Lambrechts K, et al. Xenon Blocks Neuronal Injury Associated with Decompression. Sci Rep. 2015 Oct 15. 5:15093. [Medline].
Wright PJ. Comparison of phosphodiesterase type 5 (PDE5) inhibitors. Int J Clin Pract. 2006 Aug. 60(8):967-75. [Medline].
Gempp E, Louge P, Blatteau JE, Hugon M. Risks factors for recurrent neurological decompression sickness in recreational divers: a case-control study. J Sports Med Phys Fitness. 2012 Oct. 52(5):530-6. [Medline].
Attaran RR, Ata I, Kudithipudi V, Foster L, Sorrell VL. Protocol for optimal detection and exclusion of a patent foramen ovale using transthoracic echocardiography with agitated saline microbubbles. Echocardiography. 2006 Aug. 23 (7):616-22. [Medline].
Woods TD, Patel A. A critical review of patent foramen ovale detection using saline contrast echocardiography: when bubbles lie. J Am Soc Echocardiogr. 2006 Feb. 19 (2):215-22. [Medline].
Tsivgoulis G, Stamboulis E, Sharma VK, Heliopoulos I, Voumvourakis K, Teoh HL, et al. Safety of transcranial Doppler 'bubble study' for identification of right to left shunts: an international multicentre study. J Neurol Neurosurg Psychiatry. 2011 Nov. 82 (11):1206-8. [Medline].
Smart D, Mitchell S, Wilmshurst P, Turner M, Banham N. Joint position statement on persistent foramen ovale (PFO) and diving. South Paciﬁc Underwater Medicine Society (SPUMS) and the United Kingdom Sports Diving Medical Committee (UKSDMC). Diving Hyperb Med. 2015 Jun. 45 (2):129-31. [Medline].
Wilmshurst PT. The role of persistent foramen ovale and other shunts in decompression illness. Diving Hyperb Med. 2015 Jun. 45 (2):98-104. [Medline].
Klingmann C, Rathmann N, Hausmann D, Bruckner T, Kern R. Lower risk of decompression sickness after recommendation of conservative decompression practices in divers with and without vascular right-to-left shunt. Diving Hyperb Med. 2012 Sep. 42(3):146-50. [Medline].