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Caisson disease [decompression sickness]
Classification and external resources

Two United States Navy sailors inside a decompression chamber about to undergo training
ICD-10 T70.3
ICD-9 993.3
DiseasesDB 3491
eMedicine emerg/121
MeSH C21.866.120.248

Decompression sickness (DCS; also historically or colloquially known as divers' disease, the bends or caisson disease) describes a condition arising from the precipitation of dissolved gasses into bubbles inside the body on depressurisation.[1] DCS most commonly refers to a specific type of scuba diving hazard but may be experienced in other depressurisation events such as caisson working, flying in unpressurised aircraft and extra-vehicular activity from spacecraft.

Although DCS is not a common event, its potential severity is such that much research has gone into preventing it and scuba divers use dive tables or dive computers to set limits to their exposure to pressure. Its effects may vary from joint pain and rashes, to paralysis and death. Treatment is by hyperbaric oxygen therapy in a recompression chamber. If treated early, there is a significantly higher chance of success.

Contents

Classification

DCS is usually classified by symptoms into Type I "the bends" which involves only the skin, musculoskeletal system, or lymphatic system and Type II which involves the other organs ( such as the central nervous system ) in addition to that potentially seen with Type I DCS.[2] Type II DCS thus usually has worse outcomes.[3] The usefulness of this classification in the initial assessment has been questioned as neurological symptoms may develop after the initial presentation and both Type I and Type II DCS are treated the same.[4]

Arterial gas embolism and DCS are treated very similarly because they are both the result of gas bubbles in the body.[4] Their spectra of symptoms also overlap, although those from arterial gas embolism are more severe because they often cause infarction and tissue death as noted above. In a diving context, the two are joined under the general term of decompression illness. Another term, dysbarism, encompasses decompression sickness, arterial gas embolism, and barotrauma.

Signs and symptoms

The symptoms of DCS are often summed up by "the bends", "the chokes", "the staggers", and "the tingles" representing the musculoskeletal, pulmonary, inner ear, and skin / CNS involvement seen.

While bubbles can form anywhere in the body, the bends are most frequently observed in the shoulders, elbows, knees, and ankles.

This table gives symptoms for the different DCS types. The "bends" (joint pain) accounts for about 60 to 70 percent of all altitude DCS cases, with the shoulder being the most common site. These types are classified medically as DCS I. Neurological symptoms are present in 10 to 15 percent of all DCS cases with headache and visual disturbances the most common. DCS cases with neurological symptoms are generally classified as DCS II. The "chokes" are rare and occur in less than two-percent of all DCS cases. Skin manifestations are present in about 10 to 15 percent of all DCS cases.

Signs and symptoms of decompression sickness.
DCS type Bubble location Signs & symptoms (clinical manifestations)
Bends Mostly large joints of the body
(elbows, shoulders, hip,
wrists, knees, ankles)
  • Localized deep pain, ranging from mild (a "tingle") to excruciating. Sometimes a dull ache, but rarely a sharp pain.
  • Active and passive motion of the joint aggravates the pain.
  • The pain may be reduced by bending the joint to find a more comfortable position.
  • If caused by altitude, pain can occur immediately or up to many hours later.
Skin bends Skin
  • Itching, usually around the ears, face, neck, arms, and upper torso
  • Sensation of tiny insects crawling over the skin (formication)
  • Mottled or marbled skin usually around the shoulders, upper chest and abdomen, with itching
  • Swelling of the skin, accompanied by tiny scar-like skin depressions (pitting edema)
Neurological Brain
Spinal cord
  • Abnormal sensations such as burning, stinging, and tingling around the lower chest and back
  • Symptoms may spread from the feet up and may be accompanied by ascending weakness or paralysis
  • Girdling abdominal or chest pain
Peripheral nerves
Inner Ear[5][note 1] "the staggers"
  • Loss of balance
  • Extreme vertigo
  • Hearing loss
Chokes Lungs
  • Burning deep chest pain (under the sternum)
  • Pain is aggravated by breathing
  • Shortness of breath (dyspnea)
  • Dry constant cough

The observed frequency of symptoms of DCS are as follows:[6]

DCS symptoms by frequency.
Percentage of cases Symptoms
89% local joint pain
30% leg symptoms
70% arm symptoms
5.3% dizziness
2.3% paralysis
1.6% shortness of breath
1.3% extreme fatigue
0.5% collapse/unconsciousness
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Onset

Although onset of DCS can occur rapidly after a dive, in extreme cases even before a dive has been completed, in more than half of all cases symptoms do not begin to present until over an hour following the dive. The U.S. Navy and Technical Diving International, a leading technical diver training organisation, have published a table, which indicates onset of first symptoms:[7][8]

Onset of DCS symptoms
Percentage of cases Time to the onset of first symptoms
42% within 1 hour
60% within 3 hours
83% within 8 hours
98% within 24 hours
100% within 48 hours

The table does not differentiate between types of DCS, or types of symptom.

Causes

DCS is caused by a reduction in the ambient pressure surrounding the body, as may happen when:

1. Leaving a high pressure environment

2. Ascent from depth

3. Ascent to altitude

See below:

1 Leaving a high pressure environment

Schematic of a caisson

For example: a worker comes out of a pressurized caisson or out of a mine that has been pressurized to keep water out.[1][9][10] or, an astronaut exits a space vehicle to perform a space-walk or extra-vehicular activity but the pressure in his spacesuit is lower than the pressure in the vehicle.[1][11][12][13]

The original name for DCS was caisson disease; this term was used in the 19th century, in large engineering excavations below the water table, such as with the piers of bridges and with tunnels, where caissons under pressure were used to keep water from flooding the excavations. Workers who spend time in high-pressure atmospheric pressure conditions are at risk when they return to the lower pressure outside the caisson without slowly reducing the surrounding pressure.

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.[14]

2 Ascent from depth

Typically: a diver ascends too quickly from a dive or does not carry out the required decompression stops after a long or deep dive.[1][9][15]

DCS is best known as an injury that affects ascending underwater divers who have breathed gas which is at a higher pressure than the surface pressure due to the pressure of the surrounding water. The risk of DCS increases by diving long and/or deep without slowly ascending and making the decompression stops needed to reduce the excessive pressure of inert gases in the body, although the specific risk factors are not well understood. Some divers seem more susceptible than others under identical conditions.

There have been known cases of bends in snorkellers who have made many deep dives in succession. DCS may be the cause of the disease taravana which affects South Pacific island natives who for centuries have dived by breath-holding for food and pearls.[16]

Two principal factors control the probability that a diver will suffer DCS:

  • 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).
  • 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 precipitate (come out of solution) and form "micro bubbles" in the blood.[citation needed]

The physiologist John Scott Haldane studied this problem in the early 20th century, eventually devising the method of staged, gradual decompression, whereby the pressure on the diver is released slowly enough that the nitrogen comes gradually out of solution without leading to DCS.[9][17] Bubbles form after every dive: slow ascent and decompression stops simply reduce the volume and number of the bubbles to a level at which there is no injury to the diver.[citation needed]

Severe cases of decompression sickness can lead to death. Large bubbles of gas impede the flow of oxygen-rich blood to the brain, central nervous system and other vital organs.

Even when the change in pressure causes no immediate symptoms, rapid pressure change can cause permanent bone injury called dysbaric osteonecrosis (DON) "bone cell death from pressure changes ".[18] DON can develop from a single exposure to rapid decompression. DON often affects the humerus and femoral heads and can be diagnosed from lesions visible in X-ray images of the bones.[19][20] Unfortunately, X-rays appear normal for at least 3 months after the permanent damage has occurred; it may take 4 years after the damage has occurred for its effects to become visible in the X-ray images. [1]

3 Ascent to altitude

For example: an unpressurized aircraft ascends to altitude or the cabin pressurization system of a high-flying aircraft fails [1][11][12][21] or, divers fly in any aircraft shortly after diving (note that even in a pressurized aircraft the cabin pressure is not maintained at sea-level pressure but may drop as low as 73% of sea level pressure, equivalent to standing on a mountain at 8,000 feet (2,400 m)).[1][9][11][22]

Altitude DCS may afflict people flying in inadequately pressurized aircraft at high altitude. Cabin pressurization now prevents most DCS at altitude but cabin presurization systems still fail occasionally and some people may be predisposed to the minor drop in pressure that still occurs even in pressurized aircraft.[23][24] A high altitude parachutist performing a HALO jump may develop altitude DCS if they do not flush nitrogen from the body by pre-breathing pure oxygen.[25]

Altitude DCS became a common problem in the 1930s with the development of high-altitude balloon and aircraft flights. Today, cabin pressurization systems maintain commercial aircraft cabin pressure at the equivalent altitude of 2,400 m (7,900 ft) or less, allowing safe flights up to 12,000 m (39,000 ft). DCS is very rare in healthy individuals who experience pressures equivalent to this altitude or less. However, since the pressure in the cabin is not actually maintained at sea-level pressure, there is still a small risk of DCS in susceptible individuals such as recent divers (see Scuba diving before flying below).

There is no specific altitude threshold that can be considered safe for everyone below which it can be assured that no one will develop altitude DCS, but there is very little evidence of altitude DCS occurring among healthy individuals at pressure altitudes below 5,500 m (18,000 ft) who have not been scuba diving. Individual exposures to pressure altitudes between 5,500 m (18,000 ft) and 7,500 m (24,600 ft) have shown a low occurrence of altitude DCS. A US Air Force study of altitude DCS cases reported that 87% of incidents occurred at 7,500 m (24,600 ft) or higher.[citation needed] The higher the altitude of exposure, the greater is the risk of developing altitude DCS. Although exposures to incremental altitudes above 5,500 m (18,000 ft) show an incremental risk of altitude DCS they do not show a direct relationship with the severity of the various types of DCS (see Table 1).

Ascent to altitude can happen without flying in places such as the Ethiopian and Eritrean highland, which is about 2,000 to 3,000 m (7,000 to 10,000 ft) above sea level, and the Peruvian and Bolivian altiplano and Tibet, 3,000 to 5,000 m (10,000 to 20,000 ft) above sea level.

Predisposing factors

Environmental

  • Magnitude of the pressure reduction ratio: A large pressure reduction ratio is more likely to cause DCS than a small one.[11][22][26]
  • 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.[11][26]
  • Rate of ascent: The faster the ascent, the greater the risk of developing DCS. Ascent rates greater than about 66 ft/min (NAVY Dive Manual) when diving increase the chance of DCS, particularly during the last part of an ascent to the surface. 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.[11][26]
  • 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.[11]
  • Scuba 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 very specific provisions for post-dive time at surface level before flying to allow any residual excess nitrogen to outgas. Because the atmosphere 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 dive table surface interval is not followed if flying before that surface interval and an otherwise safe dive may then exceed the dive table limits.[9][27][28][29]
  • Diving before moving to altitude: DCS can occur even without flying if the diver moves to a high-altitude location on land immediately after scuba diving—for example, a scuba diver in Eritrea who drives from the coast to the Asmara plateau at 2,400 m (7,900 ft) may be at risk of DCS.
  • Diving at altitude: Diving in water whose surface altitude is above 300 m (980 ft)—for example Lake Titicaca is at 3,800 m (12,500 ft)—without using specially calibrated high-altitude decompression tables or dive computers.[9][27][30]

Individual

Atrial septal defect (PFO) showing left-to-right shunt. A right-to-left shunt may allow bubbles to pass into the arterial circulation
  • Age: There are some reports indicating a higher risk of altitude DCS with increasing age.[1][26]
  • Previous injury: There is some indication that recent joint or limb injuries may predispose individuals to developing decompression related bubbles.[1][31]
  • Ambient temperature: There is some evidence suggesting that individual exposure to very cold ambient temperatures may increase the risk of altitude DCS.[1][26] Decompression sickness risk can be reduced by increased ambient temperature during decompression following dives in cold water.[32]
  • Body Type: Typically, a person who has a high body fat content is at greater risk of DCS.[1][26][33] Due to poor blood supply, nitrogen is stored in greater amounts in fat tissues. Although fat represents only 15 percent of a healthy male adult's body, it stores over half of the total amount of nitrogen (about 1 litre) normally dissolved in the body.
  • Alcohol consumption/dehydration: While conventional wisdom would have one believe that the after-effects of alcohol consumption increase the susceptibility to DCS through increased dehydration[26], one study concluded that alcohol consumption did not increase the risk of DCS.[34] Studies by Walder concluded that decompression sickness could be reduced in aviators when the serum surface tension was raised by drinking isotonic saline.[26][35] The high surface tension of water is generally regarded as helpful in controlling bubble size, hence avoiding dehydration is recommended by most experts.
  • 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 up to 20 percent of adults the flap does not seal, however, allowing blood through the hole when coughing or other activities raise chest pressure. In diving, this can allow venous blood with microbubbles of inert gas to return directly to the arteries (including arteries to the brain, spinal cord and heart) rather than pass through the lungs, where the bubbles would otherwise be filtered out by the lung capillary system[36]. 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, in the spinal cord it may result in paralysis, and in the heart it results in myocardial infarction (heart attack).

Mechanism

Depressurisation of the body causes excess inert gases, which were dissolved in body liquids and tissues while the body was under higher pressure, to come out of physical solution as the pressure reduces and form gas bubbles within the body. The main inert gas for those who breathe air is nitrogen. The bubbles result in the symptoms of decompression sickness.[1][9][37]

This surfacing diver must enter a recompression chamber to avoid the bends.

The amount of gas dissolved in a liquid is described by Henry's Law, which states that when the pressure of a gas over a liquid is decreased, the amount of gas dissolved in that liquid will also decrease. A good practical demonstration of Henry's Law is offered by opening a soft drink can or bottle; during the manufacture of the drink, carbon dioxide gas at higher than atmospheric pressure is sealed in the container with the liquid. Some of the gas goes into solution with the liquid due to the higher pressure. When the container is opened, the free gas can be heard escaping from the container and bubbles form in the liquid. These bubbles are the previously dissolved carbon dioxide gas coming out of solution as a result of the reduction to atmospheric pressure of the gas inside the container.

Similarly, inert gases are dissolved in body tissues and liquids while the body is under pressure, say during a scuba dive at depth. On ascent from the dive, the excess inert gas comes out of solution in a process called "outgassing" or "offgassing". Normally most offgassing occurs by gas exchange at the lungs during exhalation[9][38][39]. If inert gas is forced to come out of solution too quickly to allow outgassing at the lungs then bubbles may form in the blood stream or within solid tissues inside the body. This causes the signs and symptoms of DCS which includes itching skin, rashes, joint pain and neurological disturbance. The formation of bubbles in the skin or joints results in the milder symptoms, while large numbers of bubbles in the venous blood can cause pulmonary (lung) damage. The most severe types of DCS interrupt—and ultimately damage—spinal cord nerve function, which may lead to paralysis, sensory system failure, and death. In the presence of a right-to-left shunt, such as a patent foramen ovale (PFO), venous bubbles may migrate to the arterial system, resulting in an arterial gas embolism which may damage the brain.[4][40]

Inert gases. Nitrogen is not the only breathing gas that causes DCS. Gas mixtures such as trimix and heliox include helium, which can also be implicated in decompression sickness. Helium both enters and leaves the body faster than nitrogen, and for dives of three or more hours in duration, the body almost reaches saturation of helium. For such dives the decompression time is shorter than for nitrogen-based breathing gases such as air.[citation needed] There is some debate as to the decompression effects of helium for shorter duration dives. Most divers do longer decompressions, whereas some groups like the WKPP have been pioneering the use of shorter decompression times by including deep stops.[citation needed]

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),[41] but controlled decompression is still required to avoid DCS.[42]

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.

Decompression Illness. A gas embolism caused by the mechanical introduction of gas into the bloodstream such as via a pulmonary barotrauma injury can have many of the same symptoms as DCS. The two conditions, Arterial Gas Embolism (AGE) and Decompression Sickness (DCS) are grouped together under the name Decompression Illness (DCI) to cover the collection of general symptoms caused by depressurisation by whatever mechanism.[4][9]

Diagnosis

DCS should be suspected if any of the symptoms occurs following a drop in pressure, particularly within 36 hours of diving. In 1995, 95% of all cases reported to DAN had shown symptoms within 24 hours.[43] Severe symptoms beginning after six hours following decompression without an altitude exposure and any symptoms that occur more than 24 hours after surfacing raises suspicion of an alternative diagnosis.[44] The diagnosis is confirmed if the symptoms are relieved by recompression.[44][45] MRI or CT can frequently identify bubbles in DCS however are not as good at determining the diagnosis as a proper history of the event and description of the symptoms.[2]

Prevention

Dive tables and dive computers have been developed that help the diver choose depth and duration of decompression stops, or maximum time at depth for a particular dive profile.

Avoiding decompression sickness is not an exact science. Accidents can occur after relatively shallow and short dives. To reduce the risks, divers should avoid long and deep dives and should ascend slowly. Also, dives requiring decompression stops and dives with less than a 16 hour interval since the previous dive increase the risk of DCS. There are many additional risk factors, such as age, obesity, fatigue, use of alcohol, dehydration and a patent foramen ovale. In addition, flying at high altitude less than 24 hours after a dive can be a precipitating factor for decompression illness.

Decompression time can be significantly shortened by breathing rich nitrox (or pure oxygen in very shallow water) during the decompression phase of the dive. The reason is that the nitrogen outgases at a rate proportional to the difference between the ppN2 (partial pressure of nitrogen) in the diver's body and the ppN2 in the gas that he or she is breathing; but the likelihood of bubbles is proportional to the difference between the ppN2 in the diver's body and the total surrounding air or water pressure. Reduction in decompression requirements can 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.

Effects of breathing pure oxygen

Breathing pure oxygen to remove nitrogen from the bloodstream

One of the most significant breakthroughs in altitude DCS research was oxygen pre-breathing. Breathing pure oxygen before exposure to a low-barometric pressure environment decreases the risk of developing altitude DCS. Oxygen pre-breathing reduces the nitrogen loading in body tissues. Pre-breathing pure oxygen before starting ascent to altitude reduces the risk of altitude DCS. However, oxygen pre-breathing has to be continued without interruption with in-flight, pure oxygen to provide effective protection against altitude DCS.[11][12] Furthermore, it is very important to understand that breathing pure oxygen only during flight (ascent, en route, descent) does not decrease the risk of altitude DCS[11][12], and should not be used instead of oxygen pre-breathing.

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 only used now by military flight crews and astronauts for their protection during high altitude and space operations. It is also used by flight test crews involved with certifying aircraft.

Astronauts aboard the International Space Station preparing for Extra-vehicular activity "camp out" at low atmospheric pressure (approximately 10 psi = 700 mbar) spending 8 sleeping hours in the Quest airlock chamber before their spacewalk. Their spacesuits can operate at 4.7 psi = 330 mbar for maximum flexibility.

Treatment

a single person recompression chamber

All cases of DCS are initially treated with 100% oxygen until hyperbaric oxygen therapy can be provided (100-percent oxygen delivered in a high-pressure chamber).[46] Mild cases of the "bends" and skin bends (excluding mottled or marbled skin appearance) may disappear during descent from high altitude but still require medical evaluation. Neurological DCS, the "chokes," and skin bends with mottled or marbled skin lesions (see Table 1) should be treated with hyperbaric oxygen therapy if seen with 10 to 14 days of development.[47]

Recompression on room air was shown to be an effective treatment for minor DCS symptoms by Keays in 1909.[48] Evidence of the effectiveness of recompression therapy utilizing oxygen was first shown by Yarbrough and Behnke[49] and has since become the standard of care for treatment of DCS.[9][50] Recompression is normally carried out in a recompression chamber. In diving, a more risky alternative is in-water recompression.[51][52][53]

Oxygen first aid has been used as an emergency treatment for diving injuries for years.[9] The success of recompression therapy as well as a decrease in the number of recompression treatments required has been shown if first aid oxygen is given within four hours after surfacing.[54] Most fully closed-circuit rebreathers can deliver sustained high concentrations of oxygen-rich breathing gas and could be used as an alternative to pure open-circuit oxygen resuscitators.[citation needed]

Prognosis

Immediate first aid treatment of 100% oxygen on demand, followed by recompression at 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-up from diving accidents reported to DAN in 1987 showed 14.3% of the 268 divers surveyed "still had residual signs and symptoms from Type II DCS and 7% from Type I DCS".[55][56] Long term follow-up by Desola showed similar results with 16% permanent neurological sequalae.[57]

Epidemiology

Although all diving carries a risk of DCS, its incidence is rare with estimates of 2.8 cases per 10,000 dives with the risk 2.6 times greater for males than females.[58] The Sporting Goods Manufacturers Association has estimated that around 3.2 million divers participate at least once a year in the United States.[3] In 1999 the Divers Alert Network (DAN) has created "Project Dive Exploration" to collect data on dive profiles and incidents. From 1998 to 2002 they recorded 50,150 dives, from which 28 recompressions were required—although these will almost certainly contain incidents of arterial gas embolism (AGE)—a rate of about 0.05%.[3][59]

History

  • 1670: Robert Boyle demonstrated that a reduction in ambient pressure could lead to bubble formation in living tissue. This description of a viper in a vacuum was the first recorded description of decompression sickness.[60]
  • 1769: Giovanni Morgagni described the post mortem findings of air in cerebral circulation and surmised this was the cause of death.
  • 1840: Colonel William Pasley who was involved in the recovery of the sunk warship HMS Royal George commented that of those who had made frequent dives "not a man escaped the repeated attacks of rheumatism and cold".[61]
  • 1841: First documented case of decompression sickness, reported by a mining engineer who observed pain and muscle cramps among coal miners working in mine shafts air-pressurized to keep water out.
  • 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.[62]

The Eads Bridge. 42 workers injured by caisson disease
  • 1871: The Eads Bridge in St Louis employed 352 compressed air workers including Dr. Alphonse Jaminet as the physician in charge. There were 30 seriously injured and 12 fatalities. Dr. Jaminet developed decompression sickness and his personal description was the first such recorded.[14]
  • 1872: The similarity between decompression sickness and iatrogenic air embolism as well as the relationship between inadequate decompression and decompression sickness was noted by Friedburg. He suggested that intravascular gas was released by rapid decompression and recommended: slow compression and decompression; four hour working shifts; limit to maximum depth 44.1 psig (4 ATA); using only healthy workers; and recompression treatment for severe cases.
  • 1873: Dr. Andrew Smith first utilized the term "caisson disease" describing 110 cases of decompression sickness as the physician in charge during construction of the Brooklyn Bridge.[14][63] The project employed 600 compressed air workers. Recompression treatment was not used. The project chief engineer Washington Roebling suffered from caisson disease.[14] (He took charge after his father John Augustus Roebling died of tetanus.) Washington's wife, Emily, helped manage the construction of the bridge after his sickness confined him to his home in Brooklyn. He battled the after-effects of the disease for the rest of his life. During this project, decompression sickness became known as "The [Grecian] Bends" because afflicted individuals characteristically arched their backs: this is possibly reminiscent of a then fashionable women's dance maneuver known as the Grecian Bend or as historian David McCullough asserts in The Great Bridge it was a crude reference to "Greek" or anal sex.[64]
  • 1900: Leonard Hill used a frog model to prove that decompression causes bubbles and that recompression resolves them.[62][65] Hill advocated linear or uniform decompression profiles.[62][65] This type of decompression is used today by saturation divers. His work was financed by Augustus Siebe and the Siebe Gorman Company.[62]
An early recompression chamber
  • 1908: "The Prevention of Compressed Air Illness" was published by J. S. Haldane, Boycott and Damant recommending staged decompression.[17] These tables were accepted for use by the Royal Navy.[62]
  • 1924: The US Navy published the first standardized recompression procedure.[66]
  • 1930s: Albert R. Behnke separated the symptoms of Arterial Gas Embolism (AGE) from those of DCS.[62]
  • 1935: Albert R. Behnke et al. experimented with oxygen for recompression therapy.[62][66][67]
  • 1937: Albert R. Behnke introduced the “no-stop” decompression tables.[62]
  • 1957: Robert Workman established a new method for calculation of decompression requirements (M-values).[68]
  • 1959: The "SOS Decompression Meter", a submersible mechanical device which simulated nitrogen uptake and release, was introduced.[69]
  • 1960: F.C. Golding et al. split the classification of DCS into Type 1 and 2.[70]
  • 1982: Paul K. Weathersby, Louis D. Homer and Edward T Flynn introduce survival analysis into the study of decompression sickness.[71]
  • 1983: Orca produced the "EDGE", a personal dive computer, using a microprocessor to calculate nitrogen absorption for twelve tissue compartments.[69]
  • 1984: Albert A. Bühlmann released his book "Decompression-Decompression Sickness" which detailed his deterministic model for calculation of decompression schedules.[72]

Society and culture

Medical insurance

In the United States, it is common for medical insurance not to cover treatment for the bends that is the result of recreational diving. This is because scuba diving is an elective and "high risk" activity and treatment for decompression sickness is expensive. A typical stay in a recompression chamber will easily cost several thousand dollars, even before emergency transportation is included. Due to this, groups such as Divers Alert Network (DAN) offer medical insurance policies that specifically cover all aspects of treatment for decompression sickness at rates of less than $100 per year.

See also

References

  1. ^ a b c d e f g h i j k Vann Richard D (ed). (1989). "The Physiological Basis of Decompression". 38th Undersea and Hyperbaric Medical Society Workshop. UHMS Publication Number 75(Phys)6-1-89.: 437. http://archive.rubicon-foundation.org/6853. Retrieved 2008-05-31. 
  2. ^ a b Marx, John (2010). Rosen's emergency medicine: concepts and clinical practice 7th edition. Philadelphia, PA: Mosby/Elsevier. p. 1908. ISBN 9780323054720. 
  3. ^ a b c Pulley, Stephen A (27 November 2007). "Decompression Sickness". Medscape. http://emedicine.medscape.com/article/769717-overview. Retrieved 2009-04-17. 
  4. ^ a b c d Francis, T. James R.; D. J. Smith (1991). "Describing Decompression Illness.". 42nd Undersea and Hyperbaric Medical Society Workshop. UHMS Publication Number 79(DECO)5-15-91.. http://archive.rubicon-foundation.org/4499. Retrieved 2008-03-17. 
  5. ^ Doolette David J, Mitchell Simon J (2003). "Biophysical basis for inner ear decompression sickness". Journal of Applied Physiology 94 (6): 2145–50. doi:10.1152/japplphysiol.01090.2002 (inactive 2010-01-07). PMID 12562679. http://jap.physiology.org/cgi/content/full/94/6/2145. Retrieved 2009-07-26. 
  6. ^ Powell, Mark (2008). Deco for Divers. Southend-on-Sea: Aquapress. pp. 70. ISBN 1905492073. 
  7. ^ U.S. Navy Supervisor of Diving (2008) (PDF). U.S. Navy Diving Manual. SS521-AG-PRO-010, revision 6. vol.5. U.S. Naval Sea Systems Command. p. 20–5. http://supsalv.org/pdf/DiveMan_rev6.pdf. Retrieved 2009-06-29. 
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Bibliography

Francis, T James R; Mitchell, Simon J (2003). "10.4: Pathophysiology of Decompression Sickness". in Brubakk, Alf O; Neuman, Tom S. Bennett and Elliott's physiology and medicine of diving, 5th Revised edition. United States: Saunders Ltd. pp. 530–56. ISBN 0702025712. OCLC 51607923. 

Footnotes

  1. ^ Inner ear counter diffusion is a rare form of DCS sometimes experienced by divers engaged in extreme deep diving, caused by helium being released from the tissues but blocked by heavier nitrogen molecules. Two of the best recorded instances of it both occurred at Boesmansgat, South Africa - once to Nuno Gomes in an early world record attempt, and later to Don Shirley when he tried to rescue David Shaw on his fateful dive trying to recover the body of Deon Dreyer, who had been one of Gomes's support divers.

External links


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