Decompression sickness

When decompression sickness or disease various violations by the action of pressure or of too rapid decompression are called. The lesions occur mainly in diving accidents and are therefore also known as the bends or caisson disease called ( from the caisson ). The common cause of all of DCI is the formation of gas bubbles inside the body.

Definition

The distinction between DCS ( decompression illness, DCI) and caisson disease ( decompression sickness, DCS ) is the German translation of the terms " illness " and " Sickness" hardly expressed and is not accepted by all diving medicine. In addition, the literature DCI as shortcut for decompression illness ( decompression incident, DCI ) is used, which is then further typified by the development of symptoms.

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

To avoid the risk of decompression sickness in astronauts during spacewalks, astronauts can change before you exit through a night at reduced pressure to the pressure conditions.

The general term decompression sickness includes the damage caused by

• Gas bubble formation by excess inert gas ( usually nitrogen, in special breathing gases helium and hydrogen) = caisson disease or decompression sickness (DCS )
• Pressure -related central tear central pulmonary vessels with subsequent gasembolischen closures (arterial gas embolism bubble, AGE)

The term caisson disease (Box disease) comes from the caissons, which were increasingly used since 1870 for the preparation of foundations for bridge piers. In contrast to the hitherto usual diving bells this allowed a much longer working time, which subsequently led to a sharp increase in decompression sickness.

Cause

According to the Henry's law is the quantity of a dissolved gas in the liquid is in direct proportion to the partial pressure of the gas above the liquid. Therefore diffused at a dive to 30 m depth, for example, by the increased partial pressure of the gas in the breathing air through the alveolar capillary membranes and accordingly more nitrogen and dissolves in the blood ( the solubility increases with the ambient pressure ). The nitrogen -rich blood is then transported through the blood vessels to different tissues in the body, where the nitrogen concentration is also increased according to the Partialdruckverschiebung and increased solubility. The different tissues are referred to as decompression models in general compartments. The nitrogen enrichment in the tissues ( saturation ), as well as the subsequent release of excess nitrogen in the emergence ( desaturation ), happens at different rates, depending on the blood flow to the tissue. The strong blood brain is referred to as "fast" tissue, the less powered joints and bones as " slow" tissues. As a half-life of a tissue is defined as the time period required for this in depth to one-half of the saturation or desaturation. During the ascent, the tissue of the nitrogen that is transported and exhaled through the blood to the lungs to desaturate. In a fast ascent to the surface, while ignoring the Dekompressionsregeln, the external pressure falls quicker than it can come to the corresponding desaturation. Blood and tissue fluid will have a gas supersaturation. The nitrogen together with other dissolved gases will not be completely in solution, but they form bubbles. This is similar to the foaming when opening a soda bottle.

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

Life support and first aid

• Alerting appropriate rescue equipment (diving doctor, emergency medical services, rescue helicopter if necessary )
• If possible, administration of pure oxygen
• If unconscious: Recovery position and constant monitoring of respiratory and circulatory parameters
• Respiratory arrest and / or cardiac arrest: cardiopulmonary resuscitation
• Heat preservation ( emergency blanket )
• If patient awareness clear: Supine position, possibly lateral position ( no shock position, as this favors the intracranial pressure ( intracranial pressure ) )
• 500 to 1000 ml of fluid intake (possibly infusion therapy with crystalline and colloidal solutions )

A summary of the initial emergency care shows the Austrian Water Rescue in their diving accident leaflet.

Prevention and risk factors

With every dive, ascent rates and the Dekompressionsregeln be observed. In the cases in which, despite compliance with these rules came to acute DCI symptoms, usually one or more of the following risk factors was present:

• Acute infections of the upper respiratory tract ( common cold or allergic asthma )
• Dehydration ( eg, due to acute diarrheal diseases or inadequate fluid intake )
• Fever
• Alcohol
• Patent foramen ovale ( PFO) - a very common, but often undetected heart disease ( incidence at about 10-20 % of people ).
• Diabetes
• Seniority
• Obesity
• Stress
• Fatigue
• Muscle soreness
• High blood pressure ( hypertension)

Typing

Decompression sickness type I

In a Type I decompression sickness, the bubbles in the skin, muscles, bones or joints attach to. They cause itching there (diving fleas), tenderness of the muscles, joint pain and movement restrictions ( Bends ). These symptoms occur in 70 % of cases within the first hour after the dive, but some were also described symptoms 24 h after the dive.

Most frequently, blue-red discoloration with slight swelling of the skin, which describes the patient as " divers fleas " with intense itching. The swelling ( edema) is caused by closures of the capillaries and lymph vessels of the skin with micro- bubbles which have an increased permeability to water.

In the muscles, the bubbles pressure sensitivity and drawing pains cause. This stops a few hours and then is similar to the soreness.

Joints, bones and ligaments showing pain and disability. Most commonly, these occur in the knee joints, rarely on the elbow and shoulder. The term Bends for these symptoms comes from the stooped posture of people suffering from this occupational disease Caissonarbeiter (English: to = bend, bow ').

Immediately after the occurrence of pure oxygen to be administered. The symptoms disappear quickly usually without hyperbaric treatment. Since the DCS I often is the forerunner of dangerous DCS II, however, a pressure chamber treatment is also recommended for the symptoms subsided.

Decompression Sickness Type II

In a Type II decompression sickness, the bubbles in the brain, inner ear or spinal cord manifest from. Also closures of the blood vessels are classified by gas bubbles ( emboli ) here.

Central embolism directly cause a clouding of consciousness, sometimes unconsciousness and respiratory paralysis, because fail important brain areas. Sometimes the diver has at first a clouding of consciousness, which becomes later in a complete loss of consciousness. Likewise occur half side paralysis and isolated failures of the extremities.

Embolic closures in the spinal cord causing paralysis on both sides, sensory disturbances or urinary or rectal disorders. These occur a little later on as the central emboli and increase often of abnormal sensations in the toes to the complete paralysis two hours later.

Inner ear emboli cause nausea, dizziness, ringing in the ears and dizziness.

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

Decompression sickness type III

Long-term damage by divers are grouped under type III. Recognized as an occupational disease are so far the aseptic osteonecrosis ( AON ), hearing loss, retinal damage and neurological sequelae uncorrected DCS type II

Cause of musculoskeletal disorders and joint changes are due to the long-term saturation of these tissues. Here the dive breaks are not sufficient to completely desaturate these slow tissue. Also available microbubbles suspected that arise in professional divers in the time between emergence and exploration of the decompression chamber. These bubbles abide by the recompression " dumb ", but may cause long-term damage.

But there are also these forms of damage after a single but very long press exposure have been reported ( submarine driver of a sunken U- boat in 1931, the very long under pressure ( 36.5 m) stood before her rescue and in which 12 years later AON was detected).

Pulmonary hypertension accident AGE ( arterial gas embolism)

For a central crack the lung alveolar wins by injury to the blood- rich tissue of the lung access to the vascular system. It comes to the crossing of breathing air into the pulmonary veins. The bubbles then call after passage through the left ventricle produced embolic plugs in the end arteries of the spinal cord, brain, or even the coronary arteries. Symptoms otherwise known as DCS II

History of decompression

Already in 1670 Robert Boyle had noted that gases dissolve in liquids under pressure and it comes to gas bubbles in the liquid during sudden depressurization. This led the German Felix Hoppe- Seyler in 1857 to establish his theory of the gas bubble embolism as the cause of decompression sickness, and in 1869 published Leroy de Mericourt a medical treatise on this ( " From a physiological standpoint, the diver is a bottle of soda water "). Although already recognized Mericourt the relationship between the depth, time and speed of the ascent, but this has not translated into manageable practice instructions for the generality of the divers.

The first systematic studies in this field were carried out by the Paris Physiology Professor Paul Bert. Published in 1878 in his textbook for diver interaction of pressure, time, and air is shown. Bert was also the first that dealt with the effects of various gases on the diver and described in addition to the role of nitrogen in the bends, the dangerous role of pure oxygen under pressure. Bert described a decompression time of 20 minutes per bar pressure relief.

These recommendations formed for about 30 years, the basis for diving work (the first German -language dissertation on "Compressed Air paralysis " was released in 1889). In 1905, he examined John Scott Haldane, 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 is exclusively dependent on the pressure of CO2 on the respiratory center. He now proposed to the British Admiralty to set up a study commission for the scientific investigation of diving to get on the gas pressure research on safe working methods for divers.

Haldane was " dive " as the first goat about 60 m in the pressure chamber. He found that lean goats were less susceptible to decompression sickness than fat. This led him to the theory of different tissue classes, which vary rapidly and saturate. Basic assumption of Haldane was that the speed depends exclusively on the degree of perfusion of the tissue. On the basis of this simplified model of the human body Haldane calculated its decompression, which he first published in 1907. The tables of Haldane went - according to unique requirements of the customer ( British Navy ) - only up to 58 m.

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

After 1945, the tables of the U.S. Navy (1958 ), the one most widely used. They use 6 tissue classes with variable supersaturation factors for each decompression.

1980 saw Albert Bühlmann, that the model of parallel saturation is no longer tenable, since the tissue can leave the nitrogen only in the surrounding tissues. He has developed a model with 16 tissue classes (ZH- L16 ), which consists of linear differential equations of order 3. Newer decompression (eg Deco 2000) are based on, but the decompression has declined in importance in the era of the dive computer. This is also because decompression tables are collections of rectangular dive profiles that are irrelevant for scuba divers, because in 99.9 % of all dives no rectangular sections are immersed, is special emerged gradually and usually dive for some time even in shallower water, so stepped dive profiles are that can be covered with any table, but with mitrechnenden dive computers.

This classical approach of Bühlmann (diffusion models ) shows but according to recent findings that encouraged hundreds of thousands of dives with dive computers to days especially weaknesses, for example in terms of the formation of microbubbles. Therefore, Bühlmann tried in collaboration with the physicist Max Hahn, as well as various diving physicians and physiologists at an alternative approach to the so-called bubble models. First time in 1989, these findings were applied in the dive computer DC11 and DC12 from Scubapro. So-called yo-yo diving and repetitive dive that could lead to older models of DCS symptoms and I were resolved. DE also Younts VPM ( varying permeability model) or Bruce R. Wienke RGBM with his (reduced gradient bubble model), which is currently used in dive computers the Finnish company Suunto. After the RGBM deep stops are favored so-called, is one of which has long been postulated that they may decrease the formation of bubbles in the venous blood. The idea of ​​deep stops is not new. It says that already short stops should be placed on greater depth in order to effectively prevent the formation of smaller bubbles.

Neither the Bühlmann, nor the VP or RGB model provide absolute security against symptoms of decompression sickness, as all models only empirical in nature and assume a significant simplification of the complex processes of setting up and desaturation in the body. In particular, the newer models need further validation by medical examinations. One possibility is testing for the presence of microbubbles in the venous and arterial circulation by Doppler studies, as they are currently practiced in the context of larger studies from DAN.