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Decompression sickness

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Decompression sickness
SpecialtyEmergency medicine, hyperbaric medicine, occupational medicine Edit this on Wikidata

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, much research has gone into preventing it and scuba divers use decompression tables or dive computers to set limits to their exposure to pressure. Its effects may vary from joint pain and rash to paralysis and death. Treatment is by hyperbaric oxygen therapy in a recompression chamber. If treated early, the outcomes have a much greater chance of being good.

Classification

DCS is sometimes classified by symptom as Type I or Type II, with the latter characterised by the more severe, neurological effects.[2] More recently, the usefulness of this classification for an initial diagnosis has been questioned since neurological symptoms may develop later, and the first aid treatment is the same.[3]

Arterial gas embolism and DCS have very similar treatment because they are both the result of gas bubbles in the body.[3] 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

Bubbles can form anywhere in the body, but symptomatic sensation is 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.

Table 1. 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.
NEUROLOGICAL Brain
  • Confusion or memory loss
  • Headache
  • Spots in visual field (scotoma), tunnel vision, double vision (diplopia), or blurry vision
  • Unexplained extreme fatigue or behaviour changes
  • Seizures, dizziness, vertigo, nausea, vomiting and unconsciousness may occur, mainly due to labyrinthitis
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
CHOKES Lungs
  • Burning deep chest pain (under the sternum)
  • Pain is aggravated by breathing
  • Shortness of breath (dyspnea)
  • Dry constant cough
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)

Causes

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

  • Leaving a high pressure environment, such as found in some working environments.
  • Ascent from depth, as at the end of a scuba dive.
  • Ascent to altitude, by flying in an un-pressurized aircraft.

Leaving a high pressure environment

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.[4]

Ascent from depth

DCS is best known as an injury that affects underwater divers who breathe gas which is at a higher pressure than surface pressure. The pressure of the surrounding water increases as the diver descends and reduces as the diver ascends. The risk of DCS increases by diving long and/or deep without slowly ascending and making the decompression stops needed to eliminate the inert gases normally, 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 without equipment for food and pearls.[5]

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.[6][7] 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 bad pressure".[8] 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.[9][10] 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]

Ascent to altitude

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.

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 8,000 feet (2,400 m) or less, allowing safe flights up to 40,000 feet (12,000 m). 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 18,000 feet (5,500 m) who have not been scuba diving. Individual exposures to pressure altitudes between 18,000 feet (5,500 m) and 25,000 feet (7,600 m) have shown a low occurrence of altitude DCS. Most cases of altitude DCS occur among individuals exposed to pressure altitudes of 25,000 feet (7,600 m) or higher. A US Air Force study of altitude DCS cases reported that only 13 percent occurred below 25,000 feet (7,600 m) The higher the altitude of exposure, the greater the risk of developing altitude DCS. It is important to clarify that although exposures to incremental altitudes above 18,000 feet (5,500 m) 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 Ethiopia and Eritrea highland (8000 feet = about 1.5 miles above sea level) and the Peru and Bolivia altiplano and Tibet (2 to 3 miles above sea level).


Predisposing factors

Environmental

  • Magnitude of the pressure reduction ratio[11][12][13]: A large pressure reduction ratio is more likely to cause DCS than a small one.
  • Repetitive exposures: Repetitive dives or ascents to altitudes above 5,500 metres (18,000 ft) within a short period of time (a few hours) also increase the risk of developing altitude DCS.[11][12]
  • Rate of ascent: The faster the ascent, the greater the risk of developing altitude DCS. 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][12]
  • Time at altitude: The longer the duration of the flight to altitudes of 5,500 metres (18,000 ft) and above, the greater the risk of altitude DCS.[11]
  • Scuba diving before flying: Divers who ascend to altitude without first taking adequate time to outgas dissolved nitrogen increase their risk of developing DCS. Altitude DCS can afflict scuba divers because their dive safety tables are calibrated to sea level while the atmosphere maintained inside a pressurized aircraft on a commercial flight may be as low as the pressure equivalent to an altitude of 8,000 feet (2,400 m) above sea level [6][14][15][16]
  • 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 8,000 feet (2,400 m) may be at risk of DCS.
  • Diving at altitude: Diving in water whose surface altitude is above 1,000 feet (300 m) for example Lake Titicaca) without using specially calibrated high-altitude decompression tables or dive computer.[6][14][17]

Individual

  • Age: There are some reports indicating a higher risk of altitude DCS with increasing age.[1][12]
  • Previous injury: There is some indication that recent joint or limb injuries may predispose individuals to developing decompression related bubbles.[1][18]
  • Ambient temperature: There is some evidence suggesting that individual exposure to very cold ambient temperatures may increase the risk of altitude DCS.[1][12] Decompression sickness risk can be reduced by increased ambient temperature during decompression following dives in cold water.[19]
  • Body Type: Typically, a person who has a high body fat content is at greater risk of DCS.[1][12][20] 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[12], one study concluded that alcohol consumption did not increase the risk of DCS.[21]. Studies by Walder concluded that decompression sickness could be reduced in aviators when the serum surface tension was raised by drinking isotonic saline[12][22]. 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[23]. 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][6][24]

This typically happens in the following situations:

  • A diver ascends too quickly from a dive or does not carry out the required decompression stops after a long or deep dive.[1][6][25]
  • Divers flying in any aircraft shortly after diving. Pressurized aircraft are not risk-free since the cabin pressure is not maintained at sea-level pressure. Commercial aircraft cabin pressure may drop as low as 73% of pressure at sea level (equivalent to standing on a mountain 8,000 feet (2,400 m) above sea level).[1][6][11][13]
  • An unpressurized aircraft ascends to altitude.[1][26][27][11]
  • The cabin pressurization system of a high-flying aircraft fails.[27][11]
  • A worker comes out of a pressurized caisson or out of a mine that has been pressurized to keep water out.[1][6][28]
  • An astronaut exits a space vehicle to perform a space-walk or extra-vehicular activity where the pressure in his spacesuit is lower than the pressure in the vehicle.[1][27][11][29]
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[6][30][31]. 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.[32][3]

Inert gasses. 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),[33] but controlled decompression is still required to avoid DCS.[34]

Main article: 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.


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.[6][3]

Prevention

Decompression tables and dive computers have been developed that help the diver choose depth and duration of decompression stops for a particular dive profile at depth.

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.

Effects of breathing pure oxygen

File:Oxymask.JPG
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 promotes the elimination or washout of nitrogen from body tissues. Pre-breathing pure oxygen for 30 minutes before starting ascent to altitude reduces the risk of altitude DCS for short exposures (10 to 30 minutes only) to altitudes between 18,000 feet (5,500 m) and 43,000 feet (13,000 m). However, oxygen pre-breathing has to be continued without interruption with in-flight, pure oxygen to provide effective protection against altitude DCS.[27][11] 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[27][11], 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

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. If the signs and symptoms persist during descent or reappear at ground level, it is necessary to provide hyperbaric oxygen treatment immediately (100-percent oxygen delivered in a high-pressure chamber). Neurological DCS, the "chokes," and skin bends with mottled or marbled skin lesions (see Table 1) should always be treated with hyperbaric oxygenation. These conditions are very serious and potentially fatal if untreated.

Recompression alone was shown to be an effective treatment for minor DCS symptoms by Keays in 1909.[35] Evidence of the effectiveness of recompression therapy utilizing oxygen was first shown by Yarbrough and Behnke[36] and has since become the standard of care for treatment of DCS.[6][37] Recompression is normally carried out in a recompression chamber. In diving, a more risky alternative is in-water recompression.[38][39][40]

Oxygen first aid has been used as an emergency treatment for diving injuries for years.[6] 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.[41] 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.

Epidemiology

Although all diving carries a risk of DCS, its incidence is rare. The Sporting Goods Manufacturers Association has estimated that around 3.2 million divers participate at least once a year in the United States.[2] 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%.[42][2]

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".[43][44] Long term follow-up by Desola showed similar results with 16% permanent neurological sequalae.[45]

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.[46]
  • 1769: Giovanni Morgagni described the post mortem findings of air in cerebral circulation and surmised this was the cause of death.
  • 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.[47]

  • 1871: The St Louis Eads Bridge 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.[4]
  • 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.[4][48] The project employed 600 compressed air workers. Recompression treatment was not used. The project chief engineer Washington Roebling suffered from caisson disease.[4] (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.[49]
  • 1900: Leonard Hill used a frog model to prove that decompression causes bubbles and that recompression resolves them.[47][50]
  • 1908: "The Prevention of Compressed Air Illness" was published by J. S. Haldane, Boycott and Damant recommending staged decompression.[7] These tables were accepted for use by the Royal Navy.[47]

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.

References

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Bibliography

James, T; Francis, R; Mitchell, Simon J (2003). "10.4: Pathophysiology of Decompression Sickness". In Brubakk, Alf O; Neuman, Tom S (ed.). Bennett and Elliott's physiology and medicine of diving, 5th Revised edition. United States: Saunders Ltd. pp. 530–56. ISBN 0702025712. OCLC 51607923.{{cite book}}: CS1 maint: multiple names: authors list (link)

See also

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