Decompression sickness
Other names	Divers' disease, the bends, aerobullosis, caisson disease
Two United States Navy sailors demonstrate treatment for decompression sickness inside a decompression chamber
Specialty	Emergency medicine

Decompression sickness (DCS; also called divers' disease, the bends, aerobullosis, and caisson disease) is a medical condition caused by dissolved gases emerging from solution as bubbles inside the body tissues during decompression. DCS most commonly occurs during or soon after a decompression ascent from underwater diving, but can also result from other causes of depressurisation, such as emerging from a caisson, decompression from saturation, flying in an unpressurised aircraft at high altitude, and extravehicular activity from spacecraft. DCS and arterial gas embolism are collectively referred to as decompression illness.

Since bubbles can form in or migrate to any part of the body, DCS can produce many symptoms, and its effects may vary from joint pain and rashes to paralysis and death. DCS often causes air bubbles to settle in major joints like knees or elbows, causing individuals to bend over in excruciating pain, hence its common name, the bends. Individual susceptibility can vary from day to day, and different individuals under the same conditions may be affected differently or not at all. The classification of types of DCS according to symptoms has evolved since its original description in the 19th century. The severity of symptoms varies from barely noticeable to rapidly fatal.

Decompression sickness can occur after an exposure to increased pressure while breathing a gas with a metabolically inert component, then decompressing too fast for it to be harmlessly eliminated through respiration, or by decompression by an upward excursion from a condition of saturation by the inert breathing gas components, or by a combination of these routes. Theoretical decompression risk is controlled by the tissue compartment with the highest inert gas concentration, which for decompression from saturation is the slowest tissue to outgas.

The risk of DCS can be managed through proper decompression procedures, and contracting the condition has become uncommon. Its potential severity has driven much research to prevent it, and divers almost universally use decompression schedules or dive computers to limit their exposure and to monitor their ascent speed. If DCS is suspected, it is treated by hyperbaric oxygen therapy in a recompression chamber. Where a chamber is not accessible within a reasonable time frame, in-water recompression may be indicated for a narrow range of presentations, if there are suitably skilled personnel and appropriate equipment available on site. Diagnosis is confirmed by a positive response to the treatment. Early treatment results in a significantly higher chance of successful recovery.^[1][2]

Decompression sickness caused by a decompression from saturation can occur in decompression or upward excursions from saturation diving, ascent to high altitudes, and extravehicular activities in space. Treatment is recompression, and oxygen therapy.

Classification

DCS is classified by symptoms. The earliest descriptions of DCS used the terms: "bends" for joint or skeletal pain; "chokes" for breathing problems; and "staggers" for neurological problems.^[3] In 1960, Golding et al. introduced a simpler classification using the term "Type I ('simple')" for symptoms involving only the skin, musculoskeletal system, or lymphatic system, and "Type II ('serious')" for symptoms where other organs (such as the central nervous system) are involved.^[3] Type II DCS is considered more serious and usually has worse outcomes.^[4] This system, with minor modifications, may still be used today.^[5] Following changes to treatment methods, this classification is now much less useful in diagnosis,^[6] since neurological symptoms may develop after the initial presentation, and both Type I and Type II DCS have the same initial management.^[7]

Decompression illness and dysbarism

The term dysbarism encompasses decompression sickness, arterial gas embolism, and barotrauma, whereas decompression sickness and arterial gas embolism are commonly classified together as decompression illness when a precise diagnosis cannot be made.^[8] DCS and arterial gas embolism are treated very similarly because they are both the result of gas bubbles in the body.^[7] The U.S. Navy prescribes identical treatment for Type II DCS and arterial gas embolism.^[9] Their spectra of symptoms also overlap, although the symptoms from arterial gas embolism are generally more severe because they often arise from an infarction (blockage of blood supply and tissue death).

Signs and symptoms

While bubbles can form anywhere in the body, DCS is most frequently observed in the shoulders, elbows, knees, and ankles. Joint pain ("the bends") accounts for about 60% to 70% of all altitude DCS cases, with the shoulder being the most common site for altitude and bounce diving, and the knees and hip joints for saturation and compressed air work.^[10] Neurological symptoms are present in 10% to 15% of DCS cases with headache and visual disturbances being the most common symptom. Skin manifestations are present in about 10% to 15% of cases. Pulmonary DCS ("the chokes") is very rare in divers and has been observed much less frequently in aviators since the introduction of oxygen pre-breathing protocols.^[11] The table below shows symptoms for different DCS types.^[12]

Frequency

The relative frequencies of different symptoms of DCS observed by the U.S. Navy are as follows:^[14]

Onset

Although onset of DCS can occur rapidly after a dive, in more than half of all cases symptoms do not begin to appear for at least an hour. In extreme cases, symptoms may occur before the dive has been completed. The U.S. Navy and Technical Diving International, a leading technical diver training organization, have published a table that documents time to onset of first symptoms. The table does not differentiate between types of DCS, or types of symptom.^[15][16]

Causes

DCS is caused by a reduction in ambient pressure that results in the formation of bubbles of inert gases within tissues of the body. It may happen when leaving a high-pressure environment, ascending from depth, or ascending to altitude. A closely related condition of bubble formation in body tissues due to isobaric counterdiffusion can occur with no change of pressure.

Ascent from depth

DCS is best known as a diving disorder that affects divers having breathed gas that is at a higher pressure than the surface pressure, owing to the pressure of the surrounding water. The risk of DCS increases when diving for extended periods or at greater depth, without ascending gradually and making the decompression stops needed to slowly reduce the excess pressure of inert gases dissolved in the body. The specific risk factors are not well understood and some divers may be more susceptible than others under identical conditions.^[17][18] DCS has been confirmed in rare cases of breath-holding divers who have made a sequence of many deep dives with short surface intervals, and may be the cause of the disease called taravana by South Pacific island natives who for centuries have dived by breath-holding for food and pearls.^[19]

Two principal factors control the risk of a diver developing DCS:

1. the rate and duration of gas absorption under pressure – the deeper or longer the dive the more gas is absorbed into body tissue in higher concentrations than normal (Henry's Law);
2. the rate and duration of outgassing on depressurization – the faster the ascent and the shorter the interval between dives the less time there is for absorbed gas to be offloaded safely through the lungs, causing these gases to come out of solution and form "micro bubbles" in the blood.^[20]

Even when the change in pressure causes no immediate symptoms, rapid pressure change can cause permanent bone injury called dysbaric osteonecrosis (DON). DON can develop from a single exposure to rapid decompression.^[21]

Leaving a high-pressure environment

When workers leave a pressurized caisson or a mine that has been pressurized to keep water out, they will experience a significant reduction in ambient pressure.^[17][22] A similar pressure reduction occurs when astronauts exit a space vehicle to perform a space-walk or extra-vehicular activity, where the pressure in their spacesuit is lower than the pressure in the vehicle.^{[17][23][24][25]}

The original name for DCS was "caisson disease". This term was introduced in the 19th century, when caissons under pressure were used to keep water from flooding large engineering excavations below the water table, such as bridge supports and tunnels. Workers spending time in high ambient pressure conditions are at risk when they return to the lower pressure outside the caisson if the pressure is not reduced slowly. DCS was a major factor during construction of Eads Bridge, when 15 workers died from what was then a mysterious illness, and later during construction of the Brooklyn Bridge, where it incapacitated the project leader Washington Roebling.^[26] On the other side of the Manhattan island during construction of the Hudson River Tunnel, contractor's agent Ernest William Moir noted in 1889 that workers were dying due to decompression sickness; Moir pioneered the use of an airlock chamber for treatment.^[27]

Ascent to altitude and loss of pressure from a pressurised environment

The most common health risk on ascent to altitude is not decompression sickness but altitude sickness, or acute mountain sickness (AMS), which has an entirely different and unrelated set of causes and symptoms. AMS results not from the formation of bubbles from dissolved gasses in the body but from exposure to a low partial pressure of oxygen and alkalosis. However, passengers in unpressurized aircraft at high altitude may also be at some risk of DCS.^{[17][23][24][28]}

Altitude DCS became a problem in the 1930s with the development of high-altitude balloon and aircraft flights but not as great a problem as AMS, which drove the development of pressurized cabins, which coincidentally controlled DCS. Commercial aircraft are now required to maintain the cabin at or below a pressure altitude of 2,400 m (7,900 ft) even when flying above 12,000 m (39,000 ft). Symptoms of DCS in healthy individuals are subsequently very rare unless there is a loss of pressurization or the individual has been diving recently.^[29][30] Divers who drive up a mountain or fly shortly after diving are at particular risk even in a pressurized aircraft because the regulatory cabin altitude of 2,400 m (7,900 ft) represents only 73% of sea level pressure.^[17][23][31]

Generally, the higher the altitude the greater the risk of altitude DCS but there is no specific, maximum, safe altitude below which it never occurs. There are very few symptoms at or below 5,500 m (18,000 ft) unless the person had predisposing medical conditions or had dived recently. There is a correlation between increased altitudes above 5,500 m (18,000 ft) and the frequency of altitude DCS but there is no direct relationship with the severity of the various types of DCS. A US Air Force study reports that there are few occurrences between 5,500 m (18,000 ft) and 7,500 m (24,600 ft) and 87% of incidents occurred at or above 7,500 m (24,600 ft). ^[32] High-altitude parachutists may reduce the risk of altitude DCS if they flush nitrogen from the body by pre-breathing pure oxygen.^[33] A similar procedure is used by astronauts and cosmonauts preparing for extravehicular activity in low pressure space suits.

Predisposing factors

Although the occurrence of DCS is not easily predictable, many predisposing factors are known. They may be considered as either environmental or individual. Decompression sickness and arterial gas embolism in recreational diving are associated with certain demographic, environmental, and dive style factors. A statistical study published in 2005 tested potential risk factors: age, gender, body mass index, smoking, asthma, diabetes, cardiovascular disease, previous decompression illness, years since certification, dives in the last year, number of diving days, number of dives in a repetitive series, last dive depth, nitrox use, and drysuit use. No significant associations with risk of decompression sickness or arterial gas embolism were found for asthma, diabetes, cardiovascular disease, smoking, or body mass index. Increased depth, previous DCI, larger number of consecutive days diving, and being male were associated with higher risk for decompression sickness and arterial gas embolism. Nitrox and drysuit use, greater frequency of diving in the past year, increasing age, and years since certification were associated with lower risk, possibly as indicators of more extensive training and experience.^[34]

Environmental

The following environmental factors have been shown to increase the risk of DCS:

• the magnitude of the pressure reduction ratio – a large pressure reduction ratio is more likely to cause DCS than a small one.^[23][31][35]
• repetitive exposures – repetitive dives within a short period of time (a few hours) increase the risk of developing DCS. Repetitive ascents to altitudes above 5,500 metres (18,000 ft) within similar short periods increase the risk of developing altitude DCS.^[23][35]
• the rate of ascent – the faster the ascent the greater the risk of developing DCS. The U.S. Navy Diving Manual indicates that ascent rates greater than about 20 m/min (66 ft/min) when diving increase the chance of DCS, while recreational dive tables such as the Bühlmann tables require an ascent rate of 10 m/min (33 ft/min) with the last 6 m (20 ft) taking at least one minute.^[36] An individual exposed to a rapid decompression (high rate of ascent) above 5,500 metres (18,000 ft) has a greater risk of altitude DCS than being exposed to the same altitude but at a lower rate of ascent.^[23][35]
• the duration of exposure – the longer the duration of the dive, the greater is the risk of DCS. Longer flights, especially to altitudes of 5,500 m (18,000 ft) and above, carry a greater risk of altitude DCS.^[23]
• underwater diving before flying – divers who ascend to altitude soon after a dive increase their risk of developing DCS even if the dive itself was within the dive table safe limits. Dive tables make provisions for post-dive time at surface level before flying to allow any residual excess nitrogen to outgas. However, the pressure maintained inside even a pressurized aircraft may be as low as the pressure equivalent to an altitude of 2,400 m (7,900 ft) above sea level. Therefore, the assumption that the dive table surface interval occurs at normal atmospheric pressure is invalidated by flying during that surface interval, and an otherwise-safe dive may then exceed the dive table limits.^[37][38][39]
• diving before travelling to altitude – DCS can occur without flying if the person moves to a high-altitude location on land immediately after diving, for example, scuba divers in Eritrea who drive from the coast to the Asmara plateau at 2,400 m (7,900 ft) increase their risk of DCS.^[40]
• diving at altitude – diving in water whose surface pressure is significantly below sea level pressure – for example, Lake Titicaca is at 3,800 m (12,500 ft). Versions of decompression tables for altitudes exceeding 300 m (980 ft), or dive computers with high-altitude settings or surface pressure sensors may be used to reduce this risk.^[37][41]

Individual

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

• dehydration – Studies by Walder concluded that decompression sickness could be reduced in aviators when the serum surface tension was raised by drinking isotonic saline,^[42] and the high surface tension of water is generally regarded as helpful in controlling bubble size.^[35] Maintaining proper hydration is recommended.^[43] There is no convincing evidence that overhydration has any benefits, and it is implicated in immersion pulmonary oedema.^[44]
• patent foramen ovale – a hole between the atrial chambers of the heart in the fetus is normally closed by a flap with the first breaths at birth. In about 20% of adults the flap does not completely seal, however, allowing blood through the hole when coughing or during activities that raise chest pressure. In diving, this can allow venous blood with microbubbles of inert gas to bypass the lungs, where the bubbles would otherwise be filtered out by the lung capillary system, and return directly to the arterial system (including arteries to the brain, spinal cord and heart).^[45] In the arterial system, bubbles (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] though risk is also increased by ingassing while the diver is warm and peripherally well-perfused, and decompressing when the diver is cold.^[49]
• 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.^[50]
• 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.^[51]

Mechanism

Depressurisation causes inert gases, which were dissolved under higher pressure, to come out of physical solution and form gas bubbles within the body. These bubbles produce the symptoms of decompression sickness.^[17][52] Bubbles may form whenever the body experiences a reduction in pressure, but not all bubbles result in DCS.^[53] The amount of gas dissolved in a liquid is described by Henry's Law, which indicates that when the pressure of a gas in contact with a liquid is decreased, the amount of that gas dissolved in the liquid will also decrease proportionately.

On ascent from a dive, inert gas comes out of solution in a process called "outgassing" or "offgassing". Under normal conditions, most offgassing occurs by gas exchange in the lungs.^[54][55] If inert gas comes out of solution too quickly to allow outgassing in the lungs then bubbles may form in the blood or within the solid tissues of the body. The formation of bubbles in the skin or joints results in milder symptoms, while large numbers of bubbles in the venous blood can cause lung damage.^[56] The most severe types of DCS interrupt – and ultimately damage – spinal cord function, leading to paralysis, sensory dysfunction, or death. In the presence of a right-to-left shunt of the heart, such as a patent foramen ovale, venous bubbles may enter the arterial system, resulting in an arterial gas embolism.^[7][57] A similar effect, known as ebullism, may occur during explosive decompression, when water vapour forms bubbles in body fluids due to a dramatic reduction in environmental pressure.^[58]

Inert gases

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.^[59] 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 WKPP have been experimenting with the use of shorter decompression times by including deep stops.^[60] The balance of evidence as of 2020 does not indicate that deep stops increase decompression efficiency.

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),^[61] but controlled decompression is still required to avoid DCS.^[62]

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.^[63] 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.^[64]

Bubble formation

The location of micronuclei or where bubbles initially form is not known.^[65] The most likely mechanisms for bubble formation are tribonucleation, when two surfaces make and break contact (such as in joints), and heterogeneous nucleation, where bubbles are created at a site based on a surface in contact with the liquid. Homogeneous nucleation, where bubbles form within the liquid itself is less likely because it requires much greater pressure differences than experienced in decompression.^[65] The spontaneous formation of nanobubbles on hydrophobic surfaces is a possible source of micronuclei, but it is not yet clear if these can grow large enough to cause symptoms as they are very stable.^[65]

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.^[65]

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.^[66]

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.^[67] If the diver has a patent foramen ovale (or a shunt in the pulmonary circulation), bubbles may pass through it and bypass the pulmonary circulation to enter the arterial blood. If these bubbles are not absorbed in the arterial plasma and lodge in systemic capillaries they will block the flow of oxygenated blood to the tissues supplied by those capillaries, and those tissues will be starved of oxygen. Moon and Kisslo (1988) concluded that "the evidence suggests that the risk of serious neurological DCI or early onset DCI is increased in divers with a resting right–to-left shunt through a PFO. There is, at present, no evidence that PFO is related to mild or late onset bends.^[68] Bubbles form within other tissues as well as the blood vessels.^[67] Inert gas can diffuse into bubble nuclei between tissues. In this case, the bubbles can distort and permanently damage the tissue.^[69] As they grow, the bubbles may also compress nerves, causing pain.^[70][71] Extravascular or autochthonous bubbles usually form in slow tissues such as joints, tendons and muscle sheaths. Direct expansion causes tissue damage, with the release of histamines and their associated affects. Biochemical damage may be as important as, or more important than mechanical effects.^[67][70][72]

Bubble size and growth may be affected by several factors – gas exchange with adjacent tissues, the presence of surfactants, coalescence and disintegration by collision.^[66] Vascular bubbles may cause direct blockage, aggregate platelets and red blood cells, and trigger the coagulation process, causing local and downstream clotting.^[69]

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.^[66] 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.^[66]

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.^[73]

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.^[73] Typical acute spinal decompression injury occurs in the columns of white matter. Infarcts are characterised by a region of oedema, haemorrhage and early myelin degeneration, and are typically centred on small blood vessels. The lesions are generally discrete. Oedema usually extends to the adjacent grey matter. Microthrombi are found in the blood vessels associated with the infarcts.^[73]

Following the acute changes there is an invasion of lipid phagocytes and degeneration of adjacent neural fibres with vascular hyperplasia at the edges of the infarcts. The lipid phagocytes are later replaced by a cellular reaction of astrocytes. Vessels in surrounding areas remain patent but are collagenised.^[73] Distribution of spinal cord lesions may be related to vascular supply. There is still uncertainty regarding the aetiology of decompression sickness damage to the spinal cord.^[73]

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.^[74]

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.^[75]

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.^[76] In 1995, 95% of all cases reported to Divers Alert Network had shown symptoms within 24 hours.^[77] This window can be extended to 36 hours for ascent to altitude and 48 hours for prolonged exposure to altitude following diving.^[10] An alternative diagnosis should be suspected if severe symptoms begin more than six hours following decompression without an altitude exposure or if any symptom occurs more than 24 hours after surfacing.^[78] The diagnosis is confirmed if the symptoms are relieved by recompression.^[78][79] Although MRI or CT can frequently identify bubbles in DCS, they are not as good at determining the diagnosis as a proper history of the event and description of the symptoms.^[5]

Test of pressure

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,^[75] 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][80]

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 include skin symptoms. Cutis marmorata due to DCS may be confused with 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 actually be symptomatic of short term CNS involvement due to bubbles which form a short term gas embolism, then resolve, but which may leave residual problems which may cause relapses. These cases are thought to be under-diagnosed.^[10] Zdroj:https://en.wikipedia.org?pojem=Decompression_sickness
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