Decompression sickness

The following individual factors have been identified as possibly contributing to increased risk of DCS:

• immersion pulmonary oedema.^[44]
• arterial gas embolism) are far more dangerous because they block circulation and cause infarction (tissue death, due to local loss of blood flow). In the brain, infarction results in stroke, and in the spinal cord it may result in paralysis.^[46]
• a person's age – there are some reports indicating a higher risk of altitude DCS with increasing age.[17]^[35]
• previous injury – there is some indication that recent joint or limb injuries may predispose individuals to developing decompression-related bubbles.^[17][47]
• ambient temperature – there is some evidence suggesting that individual exposure to very cold ambient temperatures may increase the risk of altitude DCS.^[17][35] Decompression sickness risk can be reduced by increased ambient temperature during decompression following dives in cold water.^[48]
• body type – typically, a person who has a high body fat content is at greater risk of DCS.^[17][35] This is because nitrogen is five times more soluble in fat than in water, leading to greater amounts of total body dissolved nitrogen during time at pressure. Fat represents about 15–25 percent of a healthy adult's body, but stores about half of the total amount of nitrogen (about 1 litre) at normal pressures.^[49]
• alcohol consumption – although alcohol consumption increases dehydration and therefore may increase susceptibility to DCS,^[35] a 2005 study found no evidence that alcohol consumption increases the incidence of DCS.^[50]

Mechanism

Depressurisation causes

On ascent from a dive, inert gas comes out of solution in a process called "

The main inert gas in air is nitrogen, but nitrogen is not the only gas that can cause DCS. Breathing gas mixtures such as trimix and heliox include helium, which can also cause decompression sickness. Helium both enters and leaves the body faster than nitrogen, so different decompression schedules are required, but, since helium does not cause narcosis, it is preferred over nitrogen in gas mixtures for deep diving.^[58] There is some debate as to the decompression requirements for helium during short-duration dives. Most divers do longer decompressions; however, some groups like the

Any inert gas that is breathed under pressure can form bubbles when the ambient pressure decreases. Very deep dives have been made using hydrogen–oxygen mixtures (hydrox),^[60] but controlled decompression is still required to avoid DCS.^[61]

Isobaric counterdiffusion

DCS can also be caused at a constant ambient pressure when switching between gas mixtures containing different proportions of inert gas. This is known as isobaric counterdiffusion, and presents a problem for very deep dives.^[62] For example, after using a very helium-rich trimix at the deepest part of the dive, a diver will switch to mixtures containing progressively less helium and more oxygen and nitrogen during the ascent. Nitrogen diffuses into tissues 2.65 times slower than helium but is about 4.5 times more soluble. Switching between gas mixtures that have very different fractions of nitrogen and helium can result in "fast" tissues (those tissues that have a good blood supply) actually increasing their total inert gas loading. This is often found to provoke inner ear decompression sickness, as the ear seems particularly sensitive to this effect.^[63]

Bubble formation

The location of micronuclei or where bubbles initially form is not known.

Once microbubbles have formed, they can grow by either a reduction in pressure or by diffusion of gas into the gas from its surroundings. In the body, bubbles may be located within tissues or carried along with the bloodstream. The speed of blood flow within a blood vessel and the rate of delivery of blood to capillaries (perfusion) are the main factors that determine whether dissolved gas is taken up by tissue bubbles or circulation bubbles for bubble growth.^[64]

Pathophysiology

The primary provoking agent in decompression sickness is bubble formation from excess dissolved gases. Various hypotheses have been put forward for the nucleation and growth of bubbles in tissues, and for the level of supersaturation which will support bubble growth. The earliest bubble formation detected is subclinical intravascular bubbles detectable by doppler ultrasound in the venous systemic circulation. The presence of these "silent" bubbles is no guarantee that they will persist and grow to be symptomatic.^[65]

Vascular bubbles formed in the systemic capillaries may be trapped in the lung capillaries, temporarily blocking them. If this is severe, the symptom called "chokes" may occur.

Arteries may be blocked by intravascular fat aggregation. Platelets accumulate in the vicinity of bubbles. Endothelial damage may be a mechanical effect of bubble pressure on the vessel walls, a toxic effect of stabilised platelet aggregates and possibly toxic effects due to the association of lipids with the air bubbles.^[65] Protein molecules may be denatured by reorientation of the secondary and tertiary structure when non-polar groups protrude into the bubble gas and hydrophilic groups remain in the surrounding blood, which may generate a cascade of pathophysiological events with consequent production of clinical signs of decompression sickness.^[65]

The physiological effects of a reduction in environmental pressure depend on the rate of bubble growth, the site, and surface activity. A sudden release of sufficient pressure in saturated tissue results in a complete disruption of cellular organelles, while a more gradual reduction in pressure may allow accumulation of a smaller number of larger bubbles, some of which may not produce clinical signs, but still cause physiological effects typical of a blood/gas interface and mechanical effects. Gas is dissolved in all tissues, but decompression sickness is only clinically recognised in the central nervous system, bone, ears, teeth, skin and lungs.^[72]

Necrosis has frequently been reported in the lower cervical, thoracic, and upper lumbar regions of the spinal cord. A catastrophic pressure reduction from saturation produces explosive mechanical disruption of cells by local effervescence, while a more gradual pressure loss tends to produce discrete bubbles accumulated in the white matter, surrounded by a protein layer.

Dysbaric osteonecrosis lesions are typically bilateral and usually occur at both ends of the femur and at the proximal end of the humerus Symptoms are usually only present when a joint surface is involved, which typically does not occur until a long time after the causative exposure to a hyperbaric environment. The initial damage is attributed to the formation of bubbles, and one episode can be sufficient, however incidence is sporadic and generally associated with relatively long periods of hyperbaric exposure and aetiology is uncertain. Early identification of lesions by radiography is not possible, but over time areas of radiographic opacity develop in association with the damaged bone.^[73]

Diagnosis

Diagnosis of decompression sickness relies almost entirely on clinical presentation, as there are no laboratory tests that can incontrovertibly confirm or reject the diagnosis. Various blood tests have been proposed, but they are not specific for decompression sickness, they are of uncertain utility and are not in general use.^[74]

Decompression sickness should be suspected if any of the symptoms associated with the condition occurs following a drop in pressure, in particular, within 24 hours of diving.

There is no gold standard for diagnosis, and DCI experts are rare. Most of the chambers open to treatment of recreational divers and reporting to Diver's Alert Network see fewer than 10 cases per year, making it difficult for the attending doctors to develop experience in diagnosis. A method used by commercial diving supervisors when considering whether to recompress as first aid when they have a chamber on site, is known as the test of pressure. The diver is checked for contraindications to recompression, and if none are present, recompressed. If the symptoms resolve or reduce during recompression, it is considered likely that a treatment schedule will be effective. The test is not entirely reliable, and both false positives and false negatives are possible, however in the commercial diving environment it is often considered worth treating when there is doubt,^[74] and very early recompression has a history of very high success rates and reduced number of treatments needed for complete resolution and minimal sequelae.^[1][79]

Differential diagnosis

Symptoms of DCS and arterial gas embolism can be virtually indistinguishable. The most reliable way to tell the difference is based on the dive profile followed, as the probability of DCS depends on duration of exposure and magnitude of pressure, whereas AGE depends entirely on the performance of the ascent. In many cases it is not possible to distinguish between the two, but as the treatment is the same in such cases it does not usually matter.^[10]

Other conditions which may be confused with DCS include skin symptoms cutis marmorata due to DCS and skin barotrauma due to dry suit squeeze, for which no treatment is necessary. Dry suit squeeze produces lines of redness with possible bruising where the skin was pinched between folds of the suit, while the mottled effect of cutis marmorata is usually on skin where there is subcutaneous fat, and has no linear pattern.^[10]

Transient episodes of severe neurological incapacitation with rapid spontaneous recovery shortly after a dive may be attributed to hypothermia, but may be symptomatic of short term CNS involvement, which may have residual problems or relapses. These cases are thought to be under-diagnosed.^[10]

Large areas of numbness with associated weakness or paralysis, especially if a whole limb is affected, are indicative of probable brain involvement and require urgent medical attention. Paraesthesias or weakness involving a dermatome indicate probable spinal cord or spinal nerve root involvement. Although it is possible that this may have other causes, such as an injured intervertebral disk, these symptoms indicate an urgent need for medical assessment. In combination with weakness, paralysis or loss of bowel or bladder control, they indicate a medical emergency.[80]

Prevention

Underwater diving

To prevent the excess formation of bubbles that can lead to decompression sickness, divers limit their ascent rate—the recommended ascent rate used by popular decompression models is about 10 metres (33 ft) per minute—and follow a decompression schedule as necessary.

Since divers on the surface after a dive may still have excess inert gas in their bodies, decompression from any subsequent dive before this excess is eliminated needs to modify the schedule to take account of the residual gas load from the previous dive. This will result in a shorter allowable time under water without obligatory decompression stops, or an increased decompression time during the subsequent dive. The total elimination of excess gas may take many hours, and tables will indicate the time at normal pressures that is required, which may be up to 18 hours.[84]

Decompression time can be significantly shortened by breathing mixtures containing much less inert gas during the decompression phase of the dive (or pure oxygen at stops in 6 metres (20 ft) of water or less). The reason is that the inert gas outgases at a rate proportional to the difference between the partial pressure of inert gas in the diver's body and its partial pressure in the breathing gas; whereas the likelihood of bubble formation depends on the difference between the inert gas partial pressure in the diver's body and the ambient pressure. Reduction in decompression requirements can also be gained by breathing a nitrox mix during the dive, since less nitrogen will be taken into the body than during the same dive done on air.^[85]

Following a decompression schedule does not completely protect against DCS. The algorithms used are designed to reduce the probability of DCS to a very low level, but do not reduce it to zero.^[86] The mathematical implications of all current decompression models are that provided that no tissue is ingassing, longer decompression stops will decrease decompression risk, or at worst not increase it. Efficient decompression requires the diver to ascend fast enough to establish as high a decompression gradient, in as many tissues, as safely possible, without provoking the development of symptomatic bubbles. This is facilitated by the highest acceptably safe oxygen partial pressure in the breathing gas, and avoiding gas changes that could cause counterdiffusion bubble formation or growth. The development of schedules that are both safe and efficient has been complicated by the large number of variables and uncertainties, including personal variation in response under varying environmental conditions and workload, attributed to variations of body type, fitness and other risk factors.

Exposure to altitude

One of the most significant breakthroughs in the prevention of altitude DCS is oxygen pre-breathing. Breathing pure oxygen significantly reduces the nitrogen loads in body tissues by reducing the partial pressure of nitrogen in the lungs, which induces diffusion of nitrogen from the blood into the breathing gas, and this effect eventually lowers the concentration of nitrogen in the other tissues of the body. If continued for long enough, and without interruption, this provides effective protection upon exposure to low-barometric pressure environments.^[23][24] However, breathing pure oxygen during flight alone (ascent, en route, descent) does not decrease the risk of altitude DCS as the time required for ascent is generally not sufficient to significantly desaturate the slower tissues.^[23][24]

Pure aviator oxygen which has moisture removed to prevent freezing of valves at altitude is readily available and routinely used in general aviation mountain flying and at high altitudes. Most small general aviation aircraft are not pressurized, therefore oxygen use is an FAA requirement at higher altitudes.

Although pure oxygen pre-breathing is an effective method to protect against altitude DCS, it is logistically complicated and expensive for the protection of civil aviation flyers, either commercial or private. Therefore, it is currently used only by military flight crews and astronauts for protection during high-altitude and space operations. It is also used by flight test crews involved with certifying aircraft, and may also be used for high-altitude parachute jumps.

Recompression on air was shown to be an effective treatment for minor DCS symptoms by Keays in 1909.

Normobaric oxygen administered at as close to 100% as practicable is known to be beneficial based on observed bubble reduction and symptom resolution. For this reason diver training in oxygen administration, and a system for administering a high percentage of inspired oxygen at quantities sufficient for plausible evacuation scenarios is desirable. Where oxygenation may be compromised the administration rate should be adjusted to ensure that the best practicable supplementation is maintained until supplies can be replenished.[1]

A horizontal position is preferable during evacuation if possible, with the recovery position recommended for unconscious divers, as there is evidence that inert gas washout is improved in horizontal subjects, and that large arterial bubbles tend to distribute towards the head in upright positions. A head down position is thought to be harmful in DCS.^[1]

Oral hydration is recommended in fully conscious persons, and fluids should ideally be isotonic, without alcohol, carbonation or caffeine, as diving is known to cause dehydration, and rehydration is known to reduce post-dive venous gas emboli.^[1]

Intravascular rehydration is recommended if suitably competent responders are present. Glucose free

Divers should be kept comfortably warm, as warm subjects are known to eliminate gas more quickly, but overheating aggravates neurological injury.[1]

Delay of recompression

Observational evidence shows that outcomes after recompression are likely to be better after immediate recompression, which is only possible when on-site recompression is possible, although the 2004 workshop on decompression came to the conclusion that for cases with mild symptoms, a delay before recompression is unlikely to cause any worsening of long-term outcomes.^[1]

In more serious cases recompression should be done as soon as safely possible. There is some evidence that delays longer than six hours result in slower or less complete recovery, and the number of treatments required may be increased.^[1]

Transport of a symptomatic diver

Exposing a case of decompression sickness to reduced ambient pressure will cause the bubbles to expand if not constrained by a rigid local tissue environment. This can aggravate the symptoms, and should be avoided if reasonably practicable. If a diver with DCS is transported by air, cabin pressure should be kept as close to sea level atmospheric pressure as possible, preferably not more than 150 m, either by cabin pressurisation or by remaining at low altitude throughout the flight. The risk of deterioration at higher altitudes must be considered against the risk of deterioration if not transported. Some divers with symptoms or signs of mild decompression sickness may be evacuated by pressurised commercial airliner for further treatment after a surface interval of at least 24 hours. The 2004 workshop considered it unlikely for this to cause a worse outcome. Most experience has been for short flights of less than two hours. There is little known about the effects of longer flights. Where possible, pre-flight and in-flight oxygen breathing at the highest available percentage is considered best practice. Similar precautions apply to surface transport through higher altitudes.^[1]

In-water recompression

Recompression and hyperbaric oxygen administered in a recompression chamber is recognised as the definitive treatment for DCI, but when there is no readily available access to a suitable hyperbaric chamber, and if symptoms are significant or progressing, in-water recompression (IWR) with oxygen is a medically recognised option where a group of divers including the symptomatic diver already have relevant training and equipment that provides a sufficient understanding of the associated risks and allows the involved parties to collectively accept responsibility for a decision to proceed with IWR.^[79][2]

In-water recompression (IWR) or underwater oxygen treatment is the emergency treatment of decompression sickness by returning the diver underwater to help the gas bubbles in the tissues, which are causing the symptoms, to resolve. It is a procedure that exposes the diver to significant risk which should be compared with the risk associated with the other available options. Some authorities recommend that it is only to be used when the time to

Several schedules have been published for in-water recompression treatment, but little data on their efficacy is available.[1]

The decision of whether or not to attempt IWR is dependent on identifying the diver whose condition is serious enough to justify the risk, but whose clinical condition does not indicate that the risk is unacceptable. The risk may not be justified for mild DCI, if spontaneous recovery is probable whether the diver is recompressed or not, and surface oxygen is indicated for these cases. However, in these cases the risk of the recompression is also low, and early abandonment is also unlikely to cause further harm.^[1]

Contraindications

Some signs of decompression illness which suggest a risk of permanent injury are nevertheless considered contraindications for IWR. Hearing loss and vertigo displayed in isolation with no other symptoms of DCI can have been caused by inner ear barotrauma rather than DCI, and inner ear barotrauma is generally considered a contraindication for recompression. Even when caused by DCI, vertigo can make in-water treatment hazardous if accompanied by nausea and vomiting. A diver with a deteriorating level of consciousness or with a persisting reduced level of consciousness should also not be recompressed in-water nor should a diver who does not want to go back down, or with a history of oxygen toxicity in the preceding dives, or any physical injury or incapacitation which may make the procedure unsafe.^[1]

Definitive treatment

The duration of recompression treatment depends on the severity of symptoms, the dive history, the type of recompression therapy used and the patient's response to the treatment. One of the more frequently used treatment schedules is the US Navy Table 6, which provides hyperbaric oxygen therapy with a maximum pressure equivalent to 60 feet (18 m) of seawater (2.8 bar P_O2) for a total time under pressure of 288 minutes, of which 240 minutes are on oxygen and the balance are air breaks to minimise the possibility of oxygen toxicity.^[106]

A multiplace chamber is the preferred facility for treatment of decompression sickness as it allows direct physical access to the patient by medical personnel, but monoplace chambers are more widely available and should be used for treatment if a multiplace chamber is not available or transportation would cause significant delay in treatment, as the interval between onset of symptoms and recompression is important to the quality of recovery.^[107] It may be necessary to modify the optimum treatment schedule to allow use of a monoplace chamber, but this is usually better than delaying treatment. A US Navy treatment table 5 can be safely performed without air breaks if a built-in breathing system is not available.^[107] In most cases the patient can be adequately treated in a monoplace chamber at the receiving hospital.^[107]

Altitude decompression sickness

Treatment and management may vary depending on the grade or form of decompression sickness and the treating facility or organization. First aid at altitude is oxygen at the highest practicable concentration and earliest and largest practicable reduction in cabin altitude.

Ground-level 100% oxygen therapy is suggested for 2 hours following type-1 decompression sickness that occurs at altitude, if it resolves upon descent. In more severe cases, hyperbaric oxygen therapy following standard recompression protocols is indicated. Decompression sickness in aviation most commonly follows flights in non-pressurized aircraft, flights with cabin pressure fluctuations, or in individuals who fly after diving. Cases have also been reported after the use of altitude chambers. These are relatively rare clinical events.^[108]

Prognosis

Immediate treatment with 100% oxygen, followed by recompression in a hyperbaric chamber, will in most cases result in no long-term effects. However, permanent long-term injury from DCS is possible. Three-month follow-ups on diving accidents reported to DAN in 1987 showed 14.3% of the 268 divers surveyed had ongoing symptoms of Type II DCS, and 7% from Type I DCS.^[109][110] Long-term follow-ups showed similar results, with 16% having permanent neurological sequelae.^[111]

Long term effects are dependent on both initial injury, and treatment. While almost all cases will resolve more quickly with treatment, milder cases may resolve adequately over time without recompression, where the damage is minor and the damage is not significantly aggravated by lack of treatment. In some cases the cost, inconvenience, and risk to the patient may make it appropriate not to evacuate to a hyperbaric treatment facility. These cases should be assessed by a specialist in diving medicine, which can generally be done remotely by telephone or internet.^[10]

For joint pain, the likely tissues affected depend on the symptoms, and the urgency of hyperbaric treatment will depend largely on the tissues involved.^[10]

• Sharp, localised pain that is affected by movement suggests tendon or muscle injury, both of which will usually fully resolve with oxygen and anti-inflammatory medication.
• Sharp, localised pain that is not affected by movement suggests local inflammation, which will also usually fully resolve with oxygen and anti-inflammatory medication.
• Deep, non-localised pain affected by movement suggests joint capsule tension, which is likely to fully resolve with oxygen and anti-inflammatory medication, though recompression will help it to resolve faster.
• Deep, non-localised pain not affected by movement suggests bone medulla involvement, with ischaemia due to blood vessel blockage and swelling inside the bone, which is mechanistically associated with osteonecrosis, and therefore it has been strongly recommended that these symptoms are treated with hyperbaric oxygen.

Epidemiology

The incidence of decompression sickness is rare, estimated at 2.8 to 4 cases per 10,000 dives,

Around 2013, Honduras had the highest number of decompression-related deaths and disabilities in the world, caused by unsafe practices in lobster diving among the indigenous Miskito people, who face great economic pressures.^[113] At that time it was estimated that in the country over 2000 divers had been injured and 300 others had died since the 1970s.^[113]

Timeline

• 1670: Robert Boyle demonstrated that a reduction in ambient pressure could lead to bubble formation in living tissue. This description of a bubble forming in the eye of a viper subjected to a near vacuum was the first recorded description of decompression sickness.^[114]
• 1769:
  post mortem findings of air in cerebral circulation and surmised that this was the cause of death.^[115]
• 1840: Charles Pasley, who was involved in the recovery of the sunken warship HMS Royal George, commented that, of those having made frequent dives, "not a man escaped the repeated attacks of rheumatism and cold".^[116]
• 1841: First documented case of decompression sickness, reported by a mining engineer who observed pain and muscle cramps among
  mine shafts air-pressurized to keep water out.^{[citation needed}
  ]
• 1854: Decompression sickness reported and one resulting death of caisson workers on the Royal Albert Bridge.^[117]
• 1867: Panamanian pearl divers using the revolutionary Sub Marine Explorer submersible repeatedly experienced "fever" due to rapid ascents. Continued sickness led to the vessel's abandonment in 1869.^[118]
• 1870: Bauer published outcomes of 25 paralyzed caisson workers.

  From 1870 to 1910, all prominent features were established. Explanations at the time included: cold or exhaustion causing reflex spinal cord damage; electricity cause by friction on compression; or organ congestion; and vascular stasis caused by decompression.^[115]

  

• 1871: The
  St Louis employed 352 compressed air workers including Alphonse Jaminet as the physician in charge. There were 30 seriously injured and 12 fatalities. Jaminet himself developed decompression sickness and his personal description was the first such recorded.^[26] According to Divers Alert Network, in its Inert Gas Exchange, Bubbles and Decompression Theory course, this is where "bends" was first used to refer to DCS.^[119]
• 1872: The similarity between decompression sickness and
  atm
  ); using only healthy workers; and recompression treatment for severe cases.
• 1873: Andrew Smith first used the term "caisson disease" describing 110 cases of decompression sickness as the physician in charge during construction of the Brooklyn Bridge.^[26][120] The project employed 600 compressed air workers. Recompression treatment was not used. The project chief engineer Washington Roebling had caisson disease,^[26] and endured the after-effects of the disease for the rest of his life. During this project, decompression sickness became known as "The Grecian Bends" or simply "the bends" because affected individuals characteristically bent forward at the hips: this is possibly reminiscent of a then popular women's fashion and dance maneuver known as the Grecian Bend.^[26][121]
• 1890: During construction of the Hudson River Tunnel contractor's agent Ernest William Moir pioneered the use of an airlock chamber for treatment.^[27]
• 1900:
  Leonard Hill used a frog model to prove that decompression causes bubbles and that recompression resolves them.^[115][122] Hill advocated linear or uniform decompression profiles.^[115][122] This type of decompression is used today by saturation divers. His work was financed by Augustus Siebe and the Siebe Gorman Company.^[115]
• 1904: Tunnel building to and from Manhattan Island caused over 3,000 injuries and over 30 deaths which led to laws requiring PSI limits and decompression rules for "sandhogs" in the United States.[123]
• 1904: Siebe and Gorman in conjunction with Leonard Hill developed and produced a closed bell in which a diver can be decompressed at the surface.^[124]

  

• 1908: "The Prevention of Compressed Air Illness" was published by
  staged decompression.^[125] These tables were accepted for use by the Royal Navy.^[115]
• 1914–16: Experimental decompression chambers were in use on land and aboard ship.[126]^[127][128]
• 1924: The US Navy published the first standardized recompression procedure.^[129]
• 1930s:
  Albert R Behnke separated the symptoms of Arterial Gas Embolism (AGE) from those of DCS.^[115]
• 1935: Behnke et al. experimented with oxygen for recompression therapy.[115]^[129][130]
• 1937: Behnke introduced the "no-stop" decompression tables.^[115]
• 1941: Altitude DCS is treated with hyperbaric oxygen for the first time.^[131]
• 1944: US Navy published hyperbaric treatment tables "Long Air Recompression Table with Oxygen" and "Short Oxygen Recompression Table", both using 100% oxygen below 60 fsw (18 msw)
• 1945: Field results showed that the 1944 oxygen treatment table was not yet satisfactory, so a series of tests were conducted by staff from the Navy Medical Research Institute and the Navy Experimental Diving Unit using human subjects to verify and modify the treatment tables.^[91][132] Tests were conducted using the 100-foot air-oxygen treatment table and the 100-foot air treatment table, which were found to be satisfactory. Other tables were extended until they produced satisfactory results. The resulting tables were used as the standard treatment for the next 20 years, and these tables and slight modifications were adopted by other navies and industry. Over time, evidence accumulated that the success of these table for severe decompression sickness was not very good.^[91]
• 1957: Robert Workman established a new method for calculation of decompression requirements (M-values).^[133]
• 1959: The "SOS Decompression Meter", a submersible mechanical device that simulated nitrogen uptake and release, was introduced.^[134]
• 1960: FC Golding et al. split the classification of DCS into Type 1 and 2.^[135]
• 1965: Low success rates of the existing US Navy treatment tables led to the development of the oxygen treatment table by Goodman and Workman in 1965, variations of which are still in general use as the definitive treatment for most cases of decompression sickness.^[91]
• 1965: LeMessurier and Hills published a paper on A thermodynamic approach arising from a study on Torres Strait diving techniques which suggests that decompression by conventional models results in bubble formation which is then eliminated by re-dissolving at the decompression stops.^[136]
• 1976 – M.P. Spencer showed that the sensitivity of decompression testing is increased by the use of ultrasonic methods which can detect mobile venous bubbles before symptoms of DCS emerge.^[137]
• 1982: Paul K Weathersby, Louis D Homer and Edward T Flynn introduce survival analysis into the study of decompression sickness.^[138]
• 1983: Orca produced the "EDGE", a personal dive computer, using a microprocessor to calculate nitrogen absorption for twelve tissue compartments.^[134]
• 1984:
  Albert A Bühlmann released his book "Decompression–Decompression Sickness", which detailed his deterministic model for calculation of decompression schedules.^[139]
• 1989: The advent of dive computers had not been widely accepted,[140] but after the 1989 AAUS Dive computer workshop published a group consensus list of recommendations for the use of dive computers in scientific diving, most opposition to dive computers dissipated, numerous new models were introduced, the technology dramatically improved and dive computers became standard scuba diving equipment. Over time, some of the recommendations became irrelevant as the technology improved.
• 2000: HydroSpace Engineering developed the HS Explorer, a Trimix computer with optional P_O2 monitoring and twin decompression algorithms, Buhlmann, and the first full real time RGBM implementation.^[141]
• 2001: The US Navy approved the use of Cochran NAVY decompression computer with the VVAL 18 Thalmann algorithm for Special Warfare operations.^[142][143]
• By 2010: The use of dive computers for decompression status tracking was virtually ubiquitous among recreational divers and widespread in scientific diving.^[144]
• 2018: A group of diving medical experts issued a consensus guideline on pre-hospital decompression sickness management and concluded that in-water recompression is a valid and effective emergency treatment where a chamber is not available, but is only appropriate in groups that have been trained and are competent in the skills required for IWR and have appropriate equipment.^[79]
• 2023: The animal rights group, PETA, says that it has successfully lobbied the Navy to end a pair of studies that involved subjecting sheep to conditions that simulated surfacing quickly from a great depth, causing them pain and sometimes leaving the animals paralyzed or dead.^[145]

This section needs expansion with: developments since 1984: Value of deep stops challenged, effect on decompression stress shown to be generally unhelpful.. You can help by adding to it. (September 2022)

Society and culture

Economics

In the United States, it is common for

In the United Kingdom, treatment of DCS is provided by the National Health Service. This may occur either at a specialised facility or at a hyperbaric centre based within a general hospital.[147]^[148]

Other animals

Animals may also contract DCS, especially those caught in nets and rapidly brought to the surface. It has been documented in loggerhead turtles and likely in prehistoric marine animals as well.

See also

• Decompression (diving) – Pressure reduction and its effects during ascent from depth
• Decompression illness – Disorders arising from ambient pressure reduction
• Decompression theory – Theoretical modelling of decompression physiology
• Diving disorders – Physiological disorders resulting from underwater diving
• Inner ear decompression sickness – Medical condition caused by inert gas bubbles forming out of solution
• Taravana – Decompression sickness after breath-hold diving

Notes

1. ^a autochthonous: formed or originating in the place where found.

References

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5. ^ ^{a b c} Marx, p. 1908.
6. ^ Francis & Mitchell, Manifestations, p. 579.
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External links

Look up decompression sickness in Wiktionary, the free dictionary.

• Divers Alert Network: diving medicine articles Archived 8 December 2005 at the Wayback Machine
• Dive Tables from the NOAA
• CDC – Decompression Sickness and Tunnel Workers – NIOSH Workplace Safety and Health Topic
• Pathophysiology of decompression and acute dysbaric disorders
• "Decompression Sickness" on Medscape
• Norwegian Diving- and Treatment Tables. Tables and guidelines for surface orientated diving on air and nitrox. Tables and guidelines for treatment of decompression illness. Jan Risberg • Andreas Møllerløkken • Olav Sande Eftedal. 12.8.2019