Due to the gas laws that effect the diver he cannot go to any depth whenever he pleases. Almost everyone has heard of ”THE BENDS” from old movies and T.V. shows. The picture of the hard hat diver coming up in pain, in a storm, to have a cigarette before going back down to re-compress has been in more than one motion picture. The Bends or DECOMPRESSION SICKNESS is not the terrible monster of the deep waiting to grab every diver. Many people (even some divers) believe that if you dive, sooner are latter you are going to get bent, that is not true.
Decompression sickness was discovered in the 19th century by caisson workers. In the mid 1840’s hard hat diving was making itself known. About that time a wreck off Portsmouth, England was fouling the important anchorage. The British Royal Engineers allocated Colonel William Pasley the task of removing the wreck. He seized upon this opportunity to test and evaluate diving apparatuses. His project was a great success, opening the world to diving and securing its future. The project divers worked up to seven hours a day at an average depth of 65 feet. The group historian recorded that ”of the seasoned divers, not a man escaped the repeated attacks of rheumatism and cold.” This observation was the original report of what was to become known at the time as ”The Mysterious Malady.”
During this same time diving bells were increasing in size. The industrial revolution produced high-capacity air pumps capable of sufficient pressure to keep water from entering these bells. The bells evolved into dry underwater chambers allowing several men to work dry; which was of prime importance in projects such as the building of bridge footings, or constructing tunnels. These dry work rooms were known as caissons, French for ”big box.” This design was a major leap forward in engineering because it furnished ready access from the surface, and the pressure inside kept the work area dry. An air-lock was employed to pass in and out materials and change out work shifts. The use of the caisson grew rapidly. Eventually the men who worked in these big boxes were called caisson workers or just caissons.
As the use of the caisson grew the incidents of the mysterious malady also grew. Many of the caisson workers were frequently hit with dizzy spells, shortness of breath or sharp acute pain in the joints or abdomen. After a period the worker would recover but he may not be completely free of symptoms. It was also noted that those who suffered from the mysterious malady felt better while on the job. As projects got bigger and working pressures increased the physiological problems increased, not only in number of victims, but also in severity, so much so fatalities occurred frequently. After a while the mysterious malady received the logical name of Caisson Disease.
It was during the construction of the Brooklyn Bridge in New York City that the more common name ”The Bends” was used. This name came about because of the bent over posture the afflicted person assumes. French physiologist Paul Bert first discovered the cause of caissons disease in 1878. He discovered that breathing air under pressure increased the amount of nitrogen in the tissues. As long as a person remained breathing at pressure the gas stayed in solution, but when the pressure was relived, the gas came out of solution, adjusting to the new partial pressure. Applying this to the caisson worker, who quickly changed pressure, it was deduced the nitrogen returned to a gas state to rapidly, forming bubbles throughout the blood. It was concluded that these bubbles caused the wide range of signs and symptoms. If a bubble blocked an artery or vein to a vital organ death occurred or paralysis, if in the CNS.
Dr. Bert recommended that if workers returned to the surface slowly, they could decompress without serious effect. He advocated for divers to use a steady gradual ascent, but even when this was done, some divers still experienced the bends. It was also discovered that when a worker had pain it could be relived by returning to the caisson, what was called recompression. Thus not only was the cause of the mysterious malady found, but also how to avoid and treat it. Soon after this recompression chambers were designed and placed at job sites for better treatment of the bends. These chambers could be adjusted as to increasing or decreasing the pressure, based upon the individual response of the victim. The first use of these chambers was in 1879.
It was not until 1907 when Dr. J.S. Haldane, an English physiologist, conducting experiments with the Royal Navy discovered that to prevent the bends a method of gradually relieving pressure was needed. By slowly relieving the pressure on a diver, the formation of gas bubbles in the blood could be inhibited. By bringing a diver up form pressure to normal atmospheric pressure in gradual stages, instead of continuously as Bert suggested. It was hoped that this would prevent decompression sickness and was called STAGE DECOMPRESSION. Henry’s Law shows that a gas will dissolve in a liquid in proportion to the partial pressure of that gas. As pressure rises, the amount of nitrogen that the tissues will hold also rises. If the pressure doubles the amount of gas the tissue will hold also doubles, at three times the pressure the tissue will hold three times the nitrogen, and so on. Haldane used these facts to construct the first set of dive tables, establishing a method or formulary, for stage decompression. Before this the believed safe diving limit was 120 feet but Dr. Haldane method of decompression pushed that limit to around 200 feet.
The Bends, Caisson Disease, or Decompression Sickness incurs from the formation of bubbles in the tissues. These bubbles characteristically exhibit themselves on the venous side of circulation so it is referred to as Venous Gas Embolism (VGE). Some people will develop decompression sickness on no-decompression dives, within safe limits, due to assorted states in the diver or the environment, stimulating him to absorb excessive amounts of nitrogen or obstructing its release. For this reason divers should never push the tables to their limits. Any decompression sickness that originates must be treated by recompression.
The bends is the consequence of insufficient elimination of dissolved gas following exposure to pressure; depicting the combined effects of Henry, Dalton, and Boyle’s Laws of how a gas will react when put under pressure. In accordance with Henry’s Law the amount of nitrogen absorbed or released is directly proportional to the change in its partial pressure. If one liter of nitrogen is absorbed at a pressure of one ATA, then two will be absorbed at 2 ATA, and so on. This process is called nitrogen absorption. When the tissues have taken in all the nitrogen they can hold a situation called saturation exist. At sea level the body holds about one liter of dissolved nitrogen, this nitrogen is at a partial pressure equal to the partial pressure of the nitrogen in the lungs. As the partial pressure of the nitrogen increases from descending, the partial pressure increases in the lungs. Nitrogen is then absorbed to maintain a balance between the lungs and the tissues. Nitrogen will continually be absorbed until a state of equilibrium of partial pressures exist between the incoming air and all tissues of the body, at which point saturation is reached. Any changes in pressure will cause a shift and nitrogen will be absorbed or released to adjust to the new pressure, this is known as the nitrogen cycle.
The cycle of events for nitrogen absorption and elimination are the same. Only reversed in elimination (desaturation). When blood passes by the alveoli, nitrogen passes from the air into the blood to reach an equilibrium between the air and blood. When the blood reaches another tissue a similar action occurs. Nitrogen passes into the tissue until an equilibrium is reached. Blood can carry only a limited amount of nitrogen, and when it reaches a tissue it loses its nitrogen, but does so without increasing the tissue pressure very much. When the blood leaves the tissue the venous blood nitrogen pressure is equal to the new tissue pressure. When the blood returns to the lungs, again reaching an equilibrium with incoming air. When it returns to the tissue it again reaches a new equilibrium. As the pressure of the nitrogen in the tissues increases, the blood-tissue gradient decreases. This reduction slows the rate of nitrogen exchange, thus the rate nitrogen increases in the tissues slows as the process proceeds. However each passing of blood gives up some nitrogen until complete saturation is reached.
Tissues that have large blood supplies will have more nitrogen delivered to them than tissues that have poor blood supply over the same amount of time. The result of this is that saturation occurs more rapidly to tissues that have larger blood supplies. Nitrogen is about five times as soluble in fat as in water. Therefore fatty tissues require more time and more nitrogen to saturate, when compared to lean tissues. Fatty tissue has a poor blood supply making saturation very slow. Lean tissues, which have an excellent blood supply, will almost completely saturate in a few minutes, while others, like fat, will take hours to saturate.
The amount of nitrogen it takes to saturate a diver depends on the depth, and the time the diver spends at that depth. If the diver is at 3 ATM then saturation will occur once all the diver’s tissues have 3 times the nitrogen they had at surface. If a diver is of average size, he accommodates about 1 liter of dissolved nitrogen at surface, and 3 liters at 3 ATM. Sense fat retains 5 times the nitrogen of lean tissue, much of the nitrogen content will be in the fatty tissues. An obese diver will contain considerably more nitrogen than a lean one.
A fact about nitrogen saturation is that the process requires the same length of time, regardless of the nitrogen pressure or depth involved. A diver at 40 feet will require the same amount of time to saturate as a diver at 100 feet.
The process reverses for desaturation or elimination. When the partial pressure of nitrogen in the lungs reduces, as on ascending, the new pressure will induce the nitrogen to diffuse from the tissues. The blood carries the gas to the lungs where it is expired on exhalation. Some parts of the body desaturates more slowly than others for the same reasons they saturate slowly.
The major difference between desaturation and saturation is that the body will accommodate large and sudden increases in the partial pressure without ill effect. This is not true for desaturation where sudden changes can lead to problems. When the body is at 4 ATA, the partial pressure of the nitrogen will be 3.2 ATA (80% of 4 ATA). If the diver were saturated the partial pressure of the nitrogen in the tissues also would be 3.2 ATA. If the diver were to surface quickly the total pressure on the body would reduce to 1 ATA but the nitrogen in the tissues would momentarily remain at 3.2 ATA, but it will eventually come out of solution in the form of bubbles. These bubbles in the tissues and blood results in decompression sickness. Since these bubbles form in the tissues, and are picked up by the blood, they occur on the venous side of circulation, bring on the term venous gas embolism. These bubbles in the blood can block flow to vital organs damaging tissues or put pressure on them causing dysfunction.
Fortunately the tissues and blood can hold gas in solution without serious formation of bubbles. This allows a diver to ascend slowly or stop at varying depths, to allow some of the excess gas to diffuse and pass out of the body. By ascending in increments and then waiting for a period, the diver will eventually reach the surface without experiencing decompression sickness. During most diving that will be encountered a fully saturated diver will probably never be seen. In most scuba diving only those tissues that saturate rapidly will absorb any appreciable quantity of nitrogen. This nitrogen will also desaturate easily. The Navy developed a set of standard decompression tables for controlled decompression. They take into consideration depth, bottom time, and multiple dive profiles
Most dives encountered are termed no-decompression dives that means no decompression stop was necessary. However on ascent if the elimination of nitrogen fails to keep up with the pressure reduction then a point may be reached where the gas no longer stays in solution. The symptoms that result due to these bubbles are dependent on the location of the bubble.
There is a wide range of signs and symptoms. Some are subtle while others are so pronounced there is little doubt as to their cause. Rescue divers must be able to tell the differences in signs and symptoms of VGE from AGE. Symptoms of decompression sickness have been found to occur with the following frequency:
Symptoms of the Bends by Frequency
Local Joint Pain 89%
Dizziness (The Staggers) 5.3%
Shortness of Breath 1.6%
Extreme Fatigue and Pain 1.3%
Collapse with unconsciousness 0.5%
Development of symptoms while the diver is still in the water is uncommon. Symptoms usually develop a short time after a dive. In a large sampling of cases the time of onset after surfacing was:
Time of Onset of Symptoms
50% occurred within 30 minutes
85% occurred within 1 hour
95% occurred within 3 hours
1% delayed more than 6 hours
Symptoms that develop after 24 hours are probably not the result of decompression sickness. A history of the dive is necessary, the depth, and time at depth, are useful in establishing if the diver pushed the tables, or missed required decompression stops. Remember that decompression sickness can develop in divers well within the no-decompression limits, or in divers who followed all required stops. If symptoms following a dive are thought to be due to something other than decompression sickness, then a rule out (R/O) diagnosis must be used. An example would be: ”possible shoulder sprain R/O Bends”. If no other cause can be found, and doubt exists treat decompression sickness and re-compress the victim.
The most common symptom is pain, with joint pain being the most common, but others can occur. Pain is always present, even at rest. The shoulder is the most common site of pain but any of the other joints may be involved. This pain usually begins gradually and is slightly noticed, and sometimes difficult to localize. It may be a muscle ache or located in a joint. The pain will increase in intensity and be described as a deep dull ache. Pain may or may not be increased by movement of the affected limb. The victim may exhibit guarding, or holding the affected area, in positions of comfort, to reduce the pain. Abdominal pain is a classic sign of gas bubbles in the spinal column.
The most difficult type of pain to differentiate from VGE is pain due to muscle trauma or overuse. If a diver over worked a muscle in a dive, or sprained or bruised one, it could present itself the same as decompression sickness. When there is doubt, treat as VGE. Pain also can mask more significant symptoms. Drugs should never be given to control pain because it may be the only way to localize the problem and monitor treatment progress. Sharp knife like pain shooting down an extremity, or encircling the body, vague thoracic or abdominal pain, or pain moving from one area to another, should be treated as arising from the central nervous system.
Sometimes with the bends, skin rashes develop, sometimes with itching. Rashes and itching by itself may be transient and does not require decompression, however marbleization (cutis marmorata) or molting of the skin, should be treated by recompression. This type of rash starts with intense itching, progressing redness, then gives way to patchy, dark bluish discoloration of the skin. The skin may feel thickened, and in some cases the rash is raised.
Fatigue is not uncommon after dives and by itself is not treated as VGE. If it is unusually severe, then there should be cause to do a complete neurological exam. A stricken diver may feel fatigued, or weak and attribute it to working to hard. Even as weakness increases the victim may deny it and not seek help.
Neurological symptoms associated with the bends result from the involvement of the nervous system and are similar to arterial gas embolism. The occurrence of any neurological symptom after a dive should be considered a symptom of decompression sickness or air embolism unless another cause can be found, such as trauma. Neurological symptoms include numbness, tingling, and decreased sensation (sharp/dull), weakness or paralysis, and disruption of urinary function (unable) are the most common. Disturbances of higher brain function may cause amnesia, bizarre behavior or personality changes. Lightheadedness, uncoordination, and tremors may occur. Vertigo, dizziness, ringing in the ears, and loss of hearing also may occur, but they are hard to distinguish form ear trauma resulting from squeeze or reverse block.
Signs and Symptoms of The Bends
(Develop 15 min. to 12 hrs. after surfacing)
Pain in Joints
Rash on Skin
Collapse or Unconsciousness
As soon as it is believed that the victim has decompression sickness positive pressure oxygen (100%) must be given. As stated earlier the tissues maintain a partial pressure of nitrogen with the partial pressure of nitrogen in the lungs. By administering 100% oxygen the partial pressure of the nitrogen in the lungs is reduced thus speeding up recovery. Never withhold oxygen to any victim. If a diver has pushed the tables (60 ft. for 60 min.) he is within the no-decompression limits, but should be observed for one hour. Symptoms evolving during a surface interval, or a period of observation following a no-decompression dive are only treated in a chamber. Immediate transportation to a recompression chamber is indicated. Whenever a diver loses track of his bottom time, or an emergency befalls that prevents him from doing a decompression stop, he is considered to have omitted decompression. Any diver who deviates from his dive plan, fails to monitor gauges, or plans a stop and runs out of air, must have extraordinary care taken to detect decompression sickness. If the diver shows no signs (asymptomatic) of decompression sickness, omitted decompression must be made up. If he shows symptoms, prompt treatment of oxygen by demand valve, and chamber recompression must be initiated.