Predisposing factors

Environmental

• Magnitude of the pressure reduction ratio: A large pressure reduction ratio is more likely to cause DCS than a small one.

• Repetitive exposures: Repetitive dives within a short period of time (a few hours) increase the risk of developing DCS. Repetitive ascents to altitudes above within similar short periods increase the risk of developing altitude DCS.

• 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 has a greater risk of altitude DCS than being exposed to the same altitude but at a lower rate of ascent.

• Duration of exposure: The longer the duration of the dive, the greater is the risk of DCS. Longer flights, especially to altitudes of and above, carry a greater risk of altitude DCS.

• 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 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.

• 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 may be at risk of DCS.

• Diving at altitude: Diving in water whose surface altitude is above —for example Lake Titicaca is at —without using specially calibrated high-altitude decompression tables or dive computers.

Individual

• Age: There are some reports indicating a higher risk of altitude DCS with increasing age.

• Previous injury: There is some indication that recent joint or limb injuries may predispose individuals to developing decompression related bubbles.

• Ambient temperature: There is some evidence suggesting that individual exposure to very cold ambient temperatures may increase the risk of altitude DCS. Decompression sickness risk can be reduced by increased ambient temperature during decompression following dives in cold water.

• Body Type: Typically, a person who has a high body fat content is at greater risk of DCS. Due to poor blood supply, nitrogen is stored in greater amounts in fat tissues. Although fat represents only 15 percent of a normal adult 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, one study concluded that alcohol consumption did not increase the risk of DCS. Studies by Walder concluded that decompression sickness could be reduced in aviators when the serum surface tension was raised by drinking isotonic saline. 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. 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

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. 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.
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.
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.

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), but controlled decompression is still required to avoid DCS.

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 (DCI) are grouped together under the name Decompression Illness (DCI) to cover the collection of general symptoms caused by depressurisation by whatever mechanism.

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. 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. The diagnosis is confirmed if the symptoms are relieved by recompression. 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.

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. 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, 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 airlock chamber before their spacewalk. Their spacesuits can operate at 4.7 psi = 330 mbar for maximum flexibility.

Treatment

thumb|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). 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.

Recompression on room air was shown to be an effective treatment for minor DCS symptoms by Keays in 1909. Evidence of the effectiveness of recompression therapy utilizing oxygen was first shown by Yarbrough and Behnke and has since become the standard of care for treatment of DCS. Recompression is normally carried out in a recompression chamber. In diving, a more risky alternative is in-water recompression.
Oxygen first aid has been used as an emergency treatment for diving injuries for years. 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. 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.

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". Long term follow-up by Desola showed similar results with 16% permanent neurological sequalae.

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. The Sporting Goods Manufacturers Association has estimated that around 3.2 million divers participate at least once a year in the United States. 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%.

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.

• 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".

• 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.
thumb|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.

• 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. The project employed 600 compressed air workers. Recompression treatment was not used. The project chief engineer Washington Roebling suffered from caisson disease. (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.

• 1900: Leonard Hill used a frog model to prove that decompression causes bubbles and that recompression resolves them. Hill advocated linear or uniform decompression profiles. This type of decompression is used today by saturation divers. His work was financed by Augustus Siebe and the Siebe Gorman Company.

thumb|An early recompression chamber

• 1908: "The Prevention of Compressed Air Illness" was published by J. S. Haldane, Boycott and Damant recommending staged decompression. These tables were accepted for use by the Royal Navy.

• 1924: The US Navy published the first standardized recompression procedure.Thalmann, Edward D. Principles of U.S Navy recompression treatments for decompression sickness. In:

• 1930s: Albert R. Behnke separated the symptoms of Arterial Gas Embolism (AGE) from those of DCS.

• 1935: Albert R. Behnke et al. experimented with oxygen for recompression therapy.

• 1937: Albert R. Behnke introduced the “no-stop” decompression tables.

• 1957: Robert Workman established a new method for calculation of decompression requirements (M-values).

• 1959: The "SOS Decompression Meter", a submersible mechanical device which simulated nitrogen uptake and release, was introduced.

• 1960: F.C. Golding et al. split the classification of DCS into Type 1 and 2.

• 1982: Paul K. Weathersby, Louis D. Homer and Edward T Flynn introduce survival analysis into the study of decompression sickness.

• 1983: Orca produced the "EDGE", a personal dive computer, using a microprocessor to calculate nitrogen absorption for twelve tissue compartments.

• 1984: Albert A. Bühlmann released his book "Decompression-Decompression Sickness" which detailed his deterministic model for calculation of decompression schedules.

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

• Hyperbaric chamber

• Hyperbaric medicine

• Decompression illness