decompression sickness

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Classification according to ICD-10
T70.3 Caisson disease [decompression sickness]
decompression sickness
decompression sickness
ICD-10 online (WHO version 2019)

When decompression sickness or pressure diarrheal disease , various disorders are injuries due to rapid depressurization after exposure to overpressure referred. The injuries occur mainly in diving accidents ("decompression accident "), which is why the disease is also known as diving disease or caisson disease (from the French word for " caisson "). The common cause of all decompression sickness is the formation of gas bubbles inside the body ( ebullism ).


The distinction between decompression illness (DCI) and caisson sickness ( decompression sickness , DCS) is hardly expressed in the German translation of the terms “illness” and “sickness” and is not accepted by all diving doctors. In addition, DCI is also used in the literature as an abbreviation for the decompression incident (DCI), which is then further typified based on the development of the symptoms.

In English , the most common form of decompression sickness is called decompression sickness (DCS) or decompression illness (DCI). At high altitudes ( mountain lake diving ) the risk is greater due to the lower atmospheric pressure .

In order for astronauts the risk of decompression sickness in space exits to avoid astronauts be adapted to the pressure conditions in front of the exit by a night at reduced pressure.

The umbrella term decompression sickness covers the damage caused by

The term caisson disease (box disease ) comes from the caissons , which were increasingly used from 1870 to produce foundations for bridge piers. In contrast to the diving bells that had been used up until then , these enabled considerably longer working hours, which subsequently led to a sharp increase in the number of cases of decompression sickness.

root cause

According to Henry's law , the amount of gas dissolved in a liquid is directly related to the partial pressure of the gas above the liquid. Therefore diffuses during a dive on z. B. 30 m depth due to the increased partial pressure of the gas in the air, correspondingly more nitrogen through the alveolar and capillary membranes and dissolves in the blood (solubility increases with the ambient pressure). The more nitrogen-rich blood is then transported through the vessels to the various tissues in the body, where the nitrogen concentration also increases according to the partial pressure shift and the increased solubility. The various tissues are generally referred to as compartments in decompression models . The nitrogen accumulation in the tissues (saturation), as well as the later release of nitrogen when ascending (desaturation), takes place at different speeds, depending on the blood flow in the tissues. The brain , which is well supplied with blood, is referred to as “fast” tissue, the joints and bones that are less supplied with blood as “slow” tissue. The half-life of a tissue is the length of time that it requires in the depth up to half of the saturation or desaturation. During the ascent, the tissues desaturate themselves from the nitrogen that is transported via the blood to the lungs and exhaled. If the ascent to the surface is too rapid, disregarding the decompression rules, the external pressure drops faster than the corresponding desaturation can occur. Blood and tissue fluid then show gas oversaturation . The nitrogen together with all other dissolved gases then do not remain completely in solution, but they form bubbles. This is comparable to frothing when opening a soda bottle.

The resulting gas bubbles can lead to mechanical injuries in the tissue and form a gas embolism in blood vessels and thus cause a local interruption of the blood supply.

First aid, emergency life-saving measures and therapy

The Austrian Water Rescue Service shows a summary of the initial emergency care in its diving accident information sheet.

Prevention and Risk Factors

The ascent rate and the decompression rules must be observed for all dives. In those cases in which acute DCI symptoms occurred despite compliance with these rules, one or more of the following risk factors were usually present:


Type I decompression sickness

In type I decompression sickness, the blisters build up in the skin , muscles , bones, or joints . There they cause itching, tenderness of the muscles, joint pain and restricted mobility. These symptoms occur in 70% of the cases within the first hour after the dive, but sometimes symptoms were also described 24 hours after the dive.

The most common occurrences of blue-red discolouration of the skin with slight swellings, which are also called "diving fleas" when itching is severe. Microbubbles cause capillaries and lymphatic vessels to become blocked, leading to increased fluid accumulation in the tissue, a localized edema .

In the muscles , the blisters cause increased tenderness and pulling pain. This lasts for a few hours and then resembles sore muscles . Also, joints , bones and ligaments can hurt and limitations of motion occur. These occur most often in the knee joints , less often in the elbow joint and shoulder . The term "bends" (of English bend , 'bend) for these symptoms comes from the stooped posture of people suffering from this occupational disease Caissonarbeiter.

Pure oxygen should be administered immediately after the occurrence. The symptoms usually disappear quickly even without pressure chamber treatment. Since the DCS I is often the forerunner of the dangerous DCS II, a hyperbaric chamber treatment is recommended even after the symptoms subside .

Type II decompression sickness

In type II decompression sickness, bubbles manifest in the inner ear , brain, or spinal cord . Occlusions of the blood vessels by gas bubbles (aeroembolism) are also classified here.

Central gas embolism immediately causes a clouding of consciousness, sometimes also unconsciousness and respiratory paralysis, if important areas of the brain fail. Sometimes the diver initially has a clouding of consciousness that later turns into complete unconsciousness. Hemiplegia and isolated failures of the extremities can also occur.

Embolic occlusions of spinal cord vessels can cause bilateral paralysis and sensory disorders as well as, in sacral segments, urinary or rectal disorders. The symptoms that occur after central embolisms often increase from paresthesia to complete paralysis two hours later.

Inner ear embolisms cause nausea , dizziness , ringing in the ears and dizziness up to the loss of position sense .

A differentiation between DCS II and AGE (arterial gas embolism) is hardly possible for the first aider (AGE occurs immediately). The lack of differentiation is initially not essential due to the same first aid measures.

Type III decompression sickness

Long-term damage to divers is summarized under Type III. Aseptic bone necrosis (AON), hearing damage, retinal damage and neurological sequelae of unresolved DCS type II have been recognized as occupational diseases .

The cause of skeletal disorders and joint changes are due to the long-term saturation of these tissues. Here, the pauses in diving are not sufficient to completely desaturate these slow tissues. Microbubbles are also suspected, which develop in professional divers in the time between surfacing and visiting the decompression chamber. These bubbles remain “silent” due to the recompression, but can lead to long-term damage.

However, damage of this type has also been reported in the event of one-off but very long pressure exposure (submarine drivers of a submarine that sank in 1931, who were under pressure for a very long time (36.5 m) before being rescued and 12 years later AON was detected).

Pulmonary overpressure accident AGE (arterial gas embolism)

In the case of a central lung tear , the alveolar air gains access to the vascular system through the injury to the blood-rich tissue of the lungs. Breathing air passes into the pulmonary veins . After passing through the left ventricle, the air bubbles cause embolic occlusions in the end arteries of the spinal cord, the brain or the coronary arteries . Otherwise symptoms as with DCS II.

History of decompression research

Already in 1670 was Robert Boyle found himself that gases under pressure in liquids and solve case of sudden pressure release to gas bubbles come into the liquid. This led the German Felix Hoppe-Seyler in 1857 to set up his theory of gas-bubble embolism as the cause of decompression sickness, and in 1869 Leroy de Mericourt published a medical treatise on this ( "From the physiological point of view, the diver is a bottle of soda water" ). Mericourt already recognized the relationship between diving depth , diving time and the speed of the ascent, but this was not implemented in manageable practical instructions for the general public.

The first systematic investigations were carried out by the Paris physiology professor Paul Bert . In his textbook for divers, published in 1878, the interaction of pressure, time and air is shown. Bert was also the first to look into the effects of the various gases on the diver, describing the role of nitrogen in decompression sickness and the dangerous role of pure oxygen under pressure. Bert described a decompression time of 20 minutes per bar of pressure relief.

These recommendations formed the basis for diving work for about 30 years (the first German-language dissertation on “compressed air paralysis” was published in 1889). In 1905, John Scott Haldane examined the effects of "bad air" in sewers, railway tunnels and coal mines on the human organism. In the course of his research, he discovered that breathing depends exclusively on the pressure of CO 2 on the respiratory center. He now proposed to the British Admiralty to set up a study commission for scientific research into diving in order to use compressed gas research to find safe working methods for divers.

Haldane was the first to let goats "dive" around 60 m in the pressure chamber. He found that lean goats were less prone to decompression sickness than fat goats. This led him to the theory of different tissue classes, which saturate and saturate at different rates. The basic assumption of Haldane was that the speed depends exclusively on the degree of blood flow in the tissue. On the basis of this simplified model of the human body, Haldane calculated his decompression tables , which he published for the first time in 1907. The tables from Haldane went - due to clear specifications from the client (British Navy) - only up to 58 m.

This model in turn was the basis of all research for about 25 years. From 1935 it was recognized that this model only applies to a very limited depth-time range and research into possible refinements was carried out (constant supersaturation factors by Hawkins, Schilling and Hansen 1935, variable supersaturation factors by Duyer 1976, theory of silent bubbles by Hills 1971).

After 1945, the US Navy tables (1958) were most widely used. These use 6 tissue classes with variable oversaturation factors for each decompression stop.

In 1980 Albert Bühlmann recognized that the model of parallel saturation is no longer tenable, since the tissues can only release nitrogen to the surrounding tissues. From this he developed a model with 16 tissue classes (ZH-L16), which consists of 3rd order linear differential equations. Newer decompression tables (e.g. Deko 2000 ) are based on this, but the decompression table has lost its importance in the age of dive computers. This is also because decompression tables are collections of rectangular dive profiles that are irrelevant for recreational divers, because in 99.9% of all dives no rectangular profiles are dived, but successively surfaced and mostly dived for a longer period of time in shallower water, so that step-shaped dive profiles are created which cannot be covered by any table, but with dive computers that are included.

This classic approach by Bühlmann ( diffusion models ), however, shows weaknesses, for example with regard to the formation of micro gas bubbles, according to more recent findings, which above all uncovered hundreds of thousands of dives with dive computers. Therefore, Bühlmann tried in collaboration with the physicist Max Hahn, as well as various diving physicians and physiologists on an alternative approach with the so-called bubble models . In 1989 this knowledge was first applied in Scubapro's DC11 and DC12 dive computers. According to the RGBM by Bruce R. Wienke, so-called deep stops are favored, which have long been postulated that they can reduce the formation of bubbles in the venous blood. The idea of deep stops is not new. It says that short stops should be made at a greater depth in order to effectively prevent the formation of smaller blisters.

Neither the Bühlmann nor the VP model from DE Younts or the RGB model offer absolute security against symptoms of decompression sickness, since all models are only empirical in nature and assume a significant simplification of the complex processes of saturation and desaturation in the body . The newer models in particular require further validation through medical examinations. One possibility is examinations to detect microbubbles in the venous and arterial blood circulation by means of Doppler examinations , as was carried out by the DAN in 2015 as part of larger studies.

Web links

Wiktionary: Taucherflöhe  - explanations of meanings, word origins, synonyms, translations

Individual evidence

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  3. James T. Webb, Andrew A. Pilmanis, Nandini Kannan, Robert M. Olson: The Effect of Staged Decompression While Breathing 100% Oxygen on Altitude Decompression Sickness . In: erospace Medical Association, vol. 71, no7 . 2000, p. 692-698 .
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  9. ^ RE Moon: Adjuvant therapy for decompression illness . In: South Pacific Underwater Medicine Society journal . tape 28 , no. 3 , 1998, ISSN  0813-1988 .
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  11. ^ H. Schubothe: Changes in atmospheric pressure and damage and illnesses caused by a lack of oxygen. In: Ludwig Heilmeyer (ed.): Textbook of internal medicine. Springer-Verlag, Berlin / Göttingen / Heidelberg 1955; 2nd edition ibid. 1961, pp. 1184–1191, here: pp. 1185 f .: Die Druckfallkrankheit (Caisson disease).
  12. ↑ Diving accident leaflet from the Austrian Water Rescue Service
  13. a b c D. I. Fryer: Subatmospheric decompression sickness in man. Technivision Services, England 1969, ISBN 978-0-85102-023-5 , pp. 343 .
  14. ^ BC Leigh, RG Dunford: Alcohol use in scuba divers treated for diving injuries: A comparison of decompression sickness and arterial gas embolism. In: Alcoholism: Clinical and Experimental Research. 2005, 29 (Suppl.), 157A. Presented at the Annual Meeting of the Research Society on Alcoholism, Santa Barbara, California, June 2005. (online) ( Memento of February 21, 2013 in the Internet Archive )
  15. RE Moon, J. Kisslo: PFO and decompression illness: update on . In: South Pacific Underwater Medicine Society journal . tape 28 , no. 3 , 1998, ISSN  0813-1988 .
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  17. Divers FAQ. Ain't that cold, accessed on May 5, 2017 .
  18. model