Decompression Illness: What Is It and What Is The Treatment? — DAN | Divers Alert Network — Medical Dive Article Decompression Illness: What Is It and What Is The Treatment? By Dr. E.D. Thalmann, DAN Assistant Medical Director With reports by Renée Duncan, editor, and Joel Dovenbarger, vice president, DAN Medical Services NOTE: This article was published in March/April 2004. Decompression illness, or DCI, is a term used to describe illness that results from a reduction in the ambient pressure surrounding a body. A good example is what happens to your body when you&#39re surfacing after a dive. DCI encompasses two diseases, decompression sickness (DCS) and arterial gas embolism (AGE). DCS is thought to result from bubbles growing in tissue and causing local damage, while AGE results from bubbles entering the lung circulation, traveling through the arteries and causing tissue damage at a distance by blocking blood flow at the small vessel level. Who Gets DCI? Decompression illness affects scuba divers, aviators, astronauts and compressed-air workers. It occurs in approximately 1,000 U.S. scuba divers each year.

Moreover, DCI hits randomly. The main risk factor for DCI is a reduction in ambient pressure, but there are other risk factors that will increase the chance of DCI occurring. These known risk factors are deep / long dives, cold water, hard exercise at depth, and rapid ascents. Rapid ascents are closely linked to the risk of AGE. Other factors thought to increase the risk of DCI but for which evidence is not conclusive are obesity, dehydration, hard exercise immediately after surfacing, and pulmonary disease. In addition, there seem to be individual risk factors that have not yet been identified. This is why some divers seem to get DCI more frequently than others although they are following the same dive profile. Since DCI is a random event, almost any dive profile can result in DCI, no matter how safe it seems. The reason is that the risk factors, both known and unknown, can influence the probability of DCI in myriad ways. Because of this, evaluation of a diver for possible decompression illness must be made on a case-by-case basis by evaluating the diver&#39s signs and symptoms and not just based on the dive profile.

Decompression Sickness Decompression sickness (DCS, also called the bends or caisson disease) is the result of inadequate decompression following exposure to increased pressure. In some cases, the disease is mild and not an immediate threat. In other cases, serious injury does occur; when this happens, the quicker treatment begins, the better the chance for a full recovery. During a dive, the body tissues absorb nitrogen from the breathing gas in proportion to the surrounding pressure. As long as the diver remains at pressure, the gas presents no problem. If the pressure is reduced too quickly, however, the nitrogen comes out of solution and forms bubbles in the tissues and bloodstream. This commonly occurs as a result of violating or approaching too closely the diving table limits, but it can also occur even when accepted guidelines have been followed. Bubbles forming in or near joints are the presumed cause of the joint pain of a classical "bend." When high levels of bubbles occur, complex reactions can take place in the body, usually in the spinal cord or brain. Numbness, paralysis and disorders of higher cerebral function may result.

If great amounts of decompression are missed and large numbers of bubbles enter the venous bloodstream, congestive symptoms in the lung and circulatory shock can then occur. Symptoms of DCS - Skin may show a blotchy rash - Paralysis, muscle weakness - Confusion, personality changes, bizarre behavior - Amnesia, tremors - Coughing up bloody, frothy sputum - Collapse or unconsciousness Note: Symptoms and signs usually appear within 15 minutes to 12 hours after surfacing; but in severe cases, symptoms may appear before surfacing or immediately afterwards. Delayed occurrence of symptoms is rare, but it does occur, especially if air travel follows diving. Denial and Recognition The most common manifestations of DCS are joint pain and numbness or tingling. Next most common are muscular weakness and inability to empty a full bladder. Severe DCS is easy to identify because the signs and symptoms are obvious. However, most DCS manifests subtly with a minor joint ache or a paresthesia (an abnormal sensation like burning, tingling or ticking) in an extremity. In many cases these symptoms are ascribed to another cause such as overexertion, heavy lifting or even a tight wetsuit.

This delays seeking help and is why it is often noted that the first symptom of DCS is denial. Sometimes these symptoms remain mild and go away by themselves, but many times they increase in severity until it is obvious to you that something is wrong and that you need help. What happens if you don&#39t seek treatment? In severe DCS, a permanent residual handicap may result: this can be a bladder dysfunction, sexual dysfunction or muscular weakness, to name a few. In some cases of neurological DCS, there mat be permanent damage to the spinal cord, which may or may not cause symptoms. However, this type of damage may decrease the likelihood of recovery from a subsequent bout of DCS. Untreated joint pains that subside are thought to cause small areas of bone damage called osteonecrosis. Usually this will not cause symptoms unless there are many bouts of untreated DCS. If this happens, however, there may be enough damage to cause the bone to become brittle or for joints to collapse or become arthritic. Prevention of DCS Recreational divers should dive conservatively, whether they are using dive tables or computers.

Experienced divers often select a table depth (versus actual depth) of 10 feet (3 meters) deeper than called for by standard procedure. This practice is highly recommended for all divers, especially when diving in cold water or when diving under strenuous conditions. Computer divers should be cautious in approaching no-decompression limits, especially when diving deeper than 100 feet (30 meters). Avoiding the risk factors noted above (deep / long dives, exercise at depth or after a dive) will decrease the chance of DCS occurring. Exposure to altitude or flying too soon after a dive can also increase the risk of decompression sickness. DAN has recently published guidelines for flying after diving.* Arterial Gas Embolism If a diver surfaces without exhaling, air trapped in the lungs expands with ascent and may rupture lung tissue - called pulmonary barotrauma - which releases gas bubbles into the arterial circulation. This distributes them to body tissues in proportion to the blood flow. Since the brain receives the highest proportion of blood flow, it is the main target organ where bubbles may interrupt circulation if they become lodged in small arteries. This is arterial gas embolism, or AGE, considered the more serious form of DCI.

In some cases the diver may have made a panicked ascent, or he may have held his breath during ascent. However, AGE can occur even if ascent appeared completely normal, and pulmonary disease such as obstructive lung disease may increase the risk of AGE. The most dramatic presentation of air embolism is the diver who surfaces unconscious and remains so, or the diver who loses consciousness within 10 minutes of surfacing. In these cases, a true medical emergency exists, and rapid evacuation to a treatment facility is paramount. On the other hand, air embolism may cause less spectacular symptoms of neurological dysfunction, such as sensations of tingling or numbness, a sensation of weakness without obvious paralysis, or complaints of difficulty in thinking without obvious confusion in individuals who are awake and easily aroused. In these cases, there is time for a more thorough evaluation by a diving medical specialist to rule out other causes of symptoms. Like DCS, mild symptoms may be ascribed to causes other than the dive, which only delays treatment. Sometimes symptoms may resolve spontaneously and the diver will not seek treatment.

The consequences of this are similar to untreated DCS: residual damage to the brain may occur, making it more likely there will be residual symptoms after a future bout of AGE, even if the later bout is treated. Symptoms of AGE - Cessation of breathing - Death Currently cerebral gas embolism is responsible for approximately 10 percent of all DCI cases annually. AGE has decreased significantly over the past decade, however, moving from 18 percent of all cases in the late 1980s and early 1990s to much lower numbers. By 1997, the fraction had fallen to 7-8 percent. In 2001, AGE was still cited in 7-8 percent but by 2002 it had fallen to 6.6 percent of the total diving population reporting DCI. It has been speculated that one of the reasons for this decrease is the advent of dive computers, which help chart the rate of ascent, thus reminding divers to slow down. Prevention of AGE Always relax and breathe normally during ascent.

Lung conditions such as asthma, infections, cysts, tumors, scar tissue from surgery or obstructive lung disease may predispose a diver to air embolism. If you have any of these conditions, it warrants an evaluation by a physician knowledgeable in diving medicine. Treatment - Call DAN! The treatment for DCI is recompression. However, the early management of air embolism and decompression sickness is the same. Although a diver with severe DCS or an air embolism requires urgent recompression for definitive treatment, it is essential that he be stabilized at the nearest medical facility before transportation to a chamber. Early oxygen first aid is important and may reduce symptoms substantially, but this should not change the treatment plan. Symptoms of air embolism and serious decompression sickness often clear after initial oxygen breathing, but they may reappear later. Because of this, always contact DAN or a dive physician in cases of suspected DCI - even if the symptoms and signs appear to have resolved. Treatment involves compression to a treatment depth, usually 60 feet, and breathing high oxygen fraction gases at an oxygen partial pressure of between 2.8 ata (atmospheres) and 3.0 ata.

Delays in seeking treatment have a higher risk of residual symptoms; over time, the initially reversible damage may become permanent. After a delay of 24 hours or more, treatment may become ineffective and symptoms may not respond to treatment. Even if there has been a delay, however, consult a diving medical specialist before drawing any conclusions about possible treatment effectiveness. In some cases, there may be residual symptoms after a treatment. Soreness in and around a joint that was affected by DCS is common and usually resolves in a few hours. If the DCI was severe, significant residual neurological dysfunction may be present, even after the most aggressive treatment. In these cases, there may be follow-up treatments, along with physical therapy. The good news is that the usual outcome is eventual complete relief from all symptoms, provided treatment was begun promptly. Care Of The Diver With Decompression Illness I. Determine the Urgency of the Injury Make an initial evaluation at the dive site. Suspect decompression illness if any of the signs or symptoms previously described occur within 24 hours of surfacing from a dive. The initial state of the affected diver will determine the order and urgency of the actions taken. Based on a classification used by the U.S.

Navy, the diver can be placed in one of three case categories: - emergency - timely Category A - Emergency Cases Of DCI Symptoms are severe and appear rapidly, within an hour or so of surfacing. Unconsciousness may occur. Symptoms may be progressing, and the diver is obviously ill. The diver may be profoundly dizzy, have trouble breathing or have major abnormalities in consciousness. Obvious neurological injury is seen in altered consciousness, abnormal gait or weakness. These divers are obviously very sick, and a true medical emergency exists. If necessary (e.g., if the diver is unconscious), begin CPR and take immediate action to have the diver evacuated. Check for foreign bodies in the airway. If ventilatory or cardiac resuscitation is required, the injured diver must be supine (lying on the back). Vomiting in this position, however, is extremely dangerous; if it occurs, quickly turn the diver to the side until the airway is cleared and resuscitation can resume in the supine position. If available, use supplemental oxygen while administering breaths to increase the percentage of oxygen received by the injured diver.

Even if CPR is successful and the diver regains consciousness, 100 percent oxygen should be provided and continued until the diver arrives at a medical facility. If Trained Healthcare Personnel Are Available . . . ... then an intravenous (IV) infusion using isotonic fluids without dextrose should be started. An initial rapid infusion of 1 liter over 30 minutes should begin to correct any dehydration and reduce hemoconcentration. Once this is accomplished, then the rate of administration should be reduced to a 100-175 cc / hour maintenance rate. Additional 1-liter boluses may be required to further correct dehydration and maintain blood pressure but should only be given by trained healthcare personnel capable of weighing the need for further fluid with possible complications. These would include fluid overload problems and discomfort from urinary retention in divers with abnormal bladder function due to spinal cord decompression sickness. If trained personnel are available, a urinary catheter should be placed in all unconscious divers and in those who cannot urinate. Call DAN After stabilization and arrangements for evacuation, contact DAN for advice on the nearest chamber location. DAN medical experts can get in touch with the receiving facility to assist in diagnosis and, if necessary, treatment.

Do this even if the diver appears to be improving on oxygen. While awaiting evacuation, take as detailed a history as possible and try to evaluate and record the diver&#39s neurological status. These facts are useful to the receiving medical facility. If air evacuation is used, cabin pressure should be maintained near sea level and not exceed 800 feet / 244 meters unless aircraft safety is compromised. Place the diver in the lateral recumbent position, also known as the recovery position. This puts the person on one side (usually left) with head supported at a low angle and the upper leg bent at the knee. If vomiting occurs in this position, gravity will assist in keeping the airway clear. Category B - Urgent Cases Of DCI Here, the only obvious symptom is severe pain that is unchanging or has progressed slowly during the past few hours. The diver does not appear to be in distress except for the pain, and the neurological signs and symptoms are not obvious without a careful history and examination. Immediately place the injured diver on 100 percent oxygen and give fluids by mouth. Do not attempt to treat the pain with analgesics until advised to do so by medical personnel. Continue providing oxygen until arrival at the medical treatment facility.

Contact DAN or the nearest medical facility for advice on what sort of transport is necessary and where the diver should be evacuated to, even if symptoms improve or are relieved with oxygen. Emergency air transport may not be necessary in all cases. While awaiting evacuation, take as detailed a history as possible and try to evaluate and record the diver&#39s neurological status. This information will be useful to those at the receiving medical facility. If air evacuation is used, cabin pressure should be maintained near sea level and not exceed 800 feet unless aircraft safety is compromised. Category C - Timely Cases Of DCI Symptoms are either not obvious or have progressed slowly for several days. Usually the main signs or symptoms are vague complaints of pain or an abnormality of sensation; the diagnosis of DCI may be in question. Obtain as complete a diving history as possible and do a neurological evaluation. Then call DAN or the nearest medical facility for advice or go to the nearest medical facility, if nearby, for evaluation. II.

Get the Dive History If possible, obtain and document the following information for all suspected cases of DCI: - For 48 hours preceding the injury, get a description of all dives: depths / times, ascent rates, intervals between dives, breathing gases, problems or symptoms at any time before, during or after the dive; - Ask for symptom onset times and progression after the diver has surfaced from last dive; - Get a description of all first aid measures taken (including times and method of 100 percent oxygen delivery) and their effect on symptoms since the injury; - Record the results of the on-site neurological examination (described below); - Make a description of all joint or other musculoskeletal pain including: location, intensity and changes with movement or weight-bearing maneuvers; - Get a description and distribution of any rashes; and - Provide a description of any traumatic injuries before, during or after the dive. III. Conduct an On-Site Neurological Examination Information regarding the injured diver&#39s neurological status will be useful to medical personnel in not only deciding the initial course of treatment but also in the effectiveness of treatment.

Examination of an injured diver&#39s central nervous system soon after an accident may provide valuable information to the physician responsible for treatment. The On-Site Neuro Exam is easy to learn and can be done by individuals with no medical experience. Perform as much of the examination as possible, but do not let it interfere with evacuation to a medical treatment facility. The examination is given on the DAN website and is also in the DAN Dive and Travel Medical Guide. IV. Get the Injured Diver to the Nearest Medical Facility and Call DAN Call for local EMS first; then call DAN. Depending on the severity of the injury (see above), take immediate care for the diver&#39s airway, breathing and circulation and contact local EMS. After making contact with EMS, then call DAN. Call the DAN Emergency Hotline Call +1-919-684-9111 to talk to an expert in diving medicine. You may call collect. DAN medical staff is on call 24 hours a day to handle diving emergencies. When You Call the DAN Emergency Hotline: 1. Tell the operator you have a diving emergency.

The operator will either connect you directly with DAN or have someone call you back at the earliest possible moment. 2. The DAN staff member may make an immediate recommendation or call you back after making arrangements with a local physician or the DAN Regional Coordinator. DAN Regional Coordinators are familiar with chamber facilities in their area, and because they&#39re qualified in diving medicine, they make recommendations about treatment. 3. The DAN staff member or Regional Coordinator may ask you to wait by the phone while he / she makes arrangements. These plans may take 30 minutes or longer, as several phone calls may be required. This delay should not place the diver in any greater danger. However, if the situation is life-threatening, arrange to transport the diver immediately to the nearest local medical facility for immediate stabilization and assessment of his or her condition. Call the DAN Emergency Hotline (+1-919-684-9111) if you need evacuation assistance through DAN TravelAssist. A Perspective The above tries to paint an accurate picture of DCI and its consequences; you should not conclude, however, that recreational diving is likely to cause injury.

In fact, DCI is rare: researchers estimate between three and four cases of dive injuries reported for every 10,000 dives - approximately 1,000 cases per year. In addition the vast majority of the DCI cases are minor and treatment results in complete resolution with no impact on future diving activity. Like any sport, scuba diving does have injuries, and knowing how to recognize DCI will ensure that in the unlikely event it does occur, the outcome will almost always be favorable. DAN is available 24/7 to assist in getting treatment for any dive injury and has access to world-class experts in the diagnosis and treatment of DCI. Not many other sports can boast of that kind of immediate support. DAN is not resting on its laurels, though. We&#39re continuing to look for ways to reduce the number of diving accidents even further. Project Dive Exploration (PDE) is a study designed to do just this. This study trains observers to recognize DCI, and they then collect dive profile data and compile information on behavioral and health aspects. The principal goal of PDE is to establish a recreational dive database that will serve as resource research in dive safety.

To learn more about PDE, see Returning to Diving after DCI The U.S. Navy has set down rules for returning to diving after treatment. For pain-only DCI where there are no neurological symptoms, divers may begin diving two to seven days after treatment, depending on the treatment table used. If there are neurological symptoms, the diver may resume diving two to four weeks after treatment, depending on symptom severity. For very severe symptoms, the diver must be reevaluated three months after treatment and cleared by a Diving Medical Officer. The Navy&#39s guidelines are for professionals, where time off must be minimized so operations are not compromised. Guides For Sport Divers For recreational divers, where diving is not a livelihood, a more conservative approach is called for to further minimize the chance that a diving injury will recur. After pain-only DCI where there are no neurological symptoms, a minimum of two weeks without diving is recommended. If there are minor neurological symptoms, six weeks without diving is recommended. If there are severe neurological symptoms or any residual symptoms, no further diving is recommended. Even if symptoms were not severe and they resolved completely, a diver who has had multiple bouts of DCI must take special considerations.

If DCI is occurring where other divers on the same profile are DCI-free, the diver may have an increased susceptibility to DCI. In these cases, a Diving Medical Specialist must be consulted to determine if diving can be resumed safely. Remember, your good health needs to last as long as you do. ---- * See the January/February 2004 issue, "How Long to Wait? DAN Discusses Provisional Guidelines for Flying After Diving," by Richard D. Vann, Ph.D., vice president, DAN Research. ---- © DAN — Alert Diver March/April 2004 NOTE: This article has been updated to reflect the new DAN Emergency Hotline number: +1-919-684-9111. Decompression Sickness Guide: Causes, Symptoms and Treatment Options Get facts about myelofibrosis treatment options here Decompression Sickness What Is It? Decompression sickness, also called generalized barotrauma or the bends, refers to injuries caused by a rapid decrease in the pressure that surrounds you, of either air or water.

It occurs most commonly in scuba or deep-sea divers, although it also can occur during high-altitude or unpressurized air travel. However, decompression sickness is rare in pressurized aircraft, such as those used for commercial flights. When you scuba dive with compressed air, you take in extra oxygen and nitrogen. Your body uses the oxygen, but the nitrogen is dissolved into your blood, where it remains during your dive. As you swim back toward the surface after a deep dive, the water pressure around you decreases. If this transition occurs too quickly, the nitrogen does not have time to clear from your blood. Instead, it separates out of your blood and forms bubbles in your tissues or blood. It is these nitrogen bubbles that cause decompression sickness. The condition is called the bends because the joint and bone pains can be so severe they double you over. What happens inside your body during decompression sickness is similar to what happens when you open a carbonated drink. When you open the can or bottle, you decrease the pressure surrounding the beverage in the container, which causes the gas to come out of the liquid in the form of bubbles. If nitrogen bubbles form in your blood, they can damage blood vessels and block normal blood flow.

Factors that put you at higher risk of decompression sickness include: Heart muscle birth defects, including patent foramen ovale, atrial septal defect and ventricular septal defect Being older than 30 Diving in cold water Lung disease Someone with an abnormal hole or opening in the heart from a birth defect is at especially high risk of developing serious symptoms from decompression illness. Because bubbles create high blood pressure in the lungs, blood and bubbles from your veins may flow more readily through the heart's opening. This means your blood can re-circulate into arteries without first getting oxygen. An opening in the heart can also allow a relatively large air bubble (called an air embolism) to circulate into your arteries. An air embolism can cause a stroke. People with asthma or another lung disease may have thin-walled air pockets in their lungs called bullae. These pockets do not empty quickly when the persons exhales. As they return to the surface after a deep dive, air in the bullae may expand. If a bulla ruptures, it could cause a collapsed lung or allow a large air bubble (air embolism) to enter the arteries.

Symptoms Symptoms of decompression sickness include: Joint pain Weakness in arms or legs A skin rash Diagnosis Your diving history and symptoms are key factors in diagnosing decompression sickness. Blood tests and joint X-rays usually do not show any signs of the problem. Expected Duration Joint pain, the most common symptom from decompression sickness, can last for days or weeks. Prevention To minimize the risk of decompression sickness while diving: Dive and rise slowly in the water, and don't stay at your deepest depth longer than recommended. Scuba divers typically use dive tables that show how long you can remain at a given depth. Do not fly within 24 hours after diving. Don't drink alcohol before diving. Avoid hot tubs, saunas or hot baths after diving. Make sure you are well hydrated, well rested and prepared before you scuba dive. If you recently had a serious illness, injury or surgery, talk to your doctor before diving. Some people should avoid diving altogether, or should consider special risks. If you have a heart defect, it is not safe to dive. If you have asthma, a history of a ruptured lung at any time in your life or another lung disease, discuss diving safety with a doctor before deciding whether to dive.

A person who requires insulin to treat diabetes may have wide swings in blood glucose levels during a dive, and caution is advised. Avoid diving if you have a groin hernia that has not been repaired, since expanding gas in the hernia can cause symptoms. Treatment Emergency treatment for decompression sickness involves maintaining blood pressure and administering high-flow oxygen. Fluids also may be given. The person should be placed left side down and if possible the head of the bed tilted down. The optimal treatment is the use of a hyperbaric oxygen chamber, which is a high-pressure chamber in which the patient receives 100% oxygen. This treatment reverses the pressure changes that allowed gas bubbles to form in the blood stream. The treatment drives nitrogen back into its liquid form so that it can be cleared more gradually from the body over a period of hours. It is not recommended that divers with decompression sickness attempt to treat themselves with deep diving. When To Call a Professional If you experience symptoms of decompression sickness after scuba diving or flying, get to a doctor as soon as you can. Hyperbaric treatment is most successful if given within several hours after symptoms start. Prognosis Most cases of decompression sickness respond well to a single treatment with hyperbaric oxygen.

Your doctor may suggest repeated treatments if you continue to experience symptoms, especially neurological symptoms. External resources Scuba Diving: Barotrauma and Decompression Sickness Scuba Diving: Barotrauma and Decompression Sickness Outlook Barotrauma/Decompression Sickness Overview Barotrauma refers to medical problems that arise from the pressure differences between areas of the body and the environment and is a particular concern for scuba divers. Certain laws of physics apply to this topic. Boyle's law states that the product of the multiplication of pressure and volume remains a constant. As the pressure increases, the volume decreases and vice versa. As you dive deeper when scuba diving, pressure increases and this volume change in gas -filled spaces and organs within your body accounts for the distortion and damage to surrounding tissues. Decompression sickness, or "the bends ," is related more to Henry's Law, which states that more gas will be dissolved in a liquid when the gas is pressurized. Because of the water pressure, body tissue absorbs nitrogen gas faster as a diver descends than when ascending to the surface. However, if a diver ascends too quickly, nitrogen gas bubbles will form in body tissue rather than being exhaled.

The nitrogen bubbles cause severe pain . External ear squeeze occurs when your ear canal is blocked by something such as earplugs or earwax . As the water pressure increases while you descend, the air pocket between the obstruction and the tympanic membrane (eardrum) shrinks. This can damage the tissue in the ear canal, usually your eardrum. Middle ear squeeze occurs when you cannot equalize the pressure in your middle ear . The eustachian tube is a small canal that connects the middle ear to the back part of the nasal cavities and allows pressure to equalize. When there is a problem with the tube, the middle ear volume decreases and pulls the eardrum inward, creating damage and pain . You can try certain maneuvers, called Valsalva maneuvers, such as yawning or trying to blow with your nose and mouth closed, to open the tube and equalize the pressure. Inner ear barotrauma occurs from the sudden development of pressure differences between the middle and inner ear. This can result from an overly forceful Valsalva maneuver or a very rapid descent. The result is usually ringing in the ear , dizziness , and deafness. This injury is less common than a middle ear squeeze .

Less common types of barotrauma include the following. All involve air trapped in an enclosed area where pressure cannot equalize during descent causing a vacuum effect where it occurs. Sinus squeeze: When air becomes trapped in the sinuses because of congestion or cold symptoms, a sinus squeeze can occur. Face mask squeeze: This occurs if you do not exhale through your nose into the dive mask while descending (equalizing). Suit squeeze: A dry diving suit tightly encloses an area of skin. Lung squeeze: This occurs when you are free-diving, but very few divers can hold their breath to depths that cause this injury to occur. Tooth squeeze: This occurs during an ascent while scuba diving and air becomes trapped in a filling or cavity. Gastric squeeze (aerogastralgia): This occurs when gas swallowed during diving expands during ascent. This happens more often with novice divers and causes temporary pain but rarely significant damage. Barotrauma can occur during ascent also. A reverse squeeze occurs in the middle ear or sinus when a diver has an upper respiratory infection (cold) and has used nasal spray to open the breathing passages. As the spray wears off during diving, tissues swell and cause obstruction, resulting in a pressure difference and damage.

During "bounce diving" the eustachian tube may become inflamed and lead to a middle ear squeeze. Pulmonary barotrauma (pulmonary overpressurization syndrome, POPS, or burst lung) can occur if the diver fails to expel air from the lungs during ascent. As the diver rises, the volume of the gas in the lung expands and can cause damage if the excess is not exhaled. Air embolism is the most serious and most feared consequence of diving. While scuba diving, gas bubbles can enter the circulatory system through small ruptured veins in the lungs. These bubbles expand during ascent, following Boyle's Law, and can pass through the heart to obstruct blood flow in the arteries of the brain or heart. This most commonly occurs when a diver ascends rapidly because of air shortage or panic. The diver then passes out, experiences a stroke , or has other nervous system complaints within minutes of surfacing. The brain is affected more than other organs because gas rises, and most divers are in a vertical position while ascending. Decompression sickness (DCS, "the bends") involves gases diffusing into the tissues and getting trapped there. The diver now has gas bubbles in places where there should be none.

Nitrogen is the usual culprit. During descent and while on the bottom, the diver absorbs nitrogen into the tissues until they reach a pressure balance. When the diver ascends at the right rate, the gas diffuses from the tissues. However, if the diver ascends too rapidly to allow diffusion, the nitrogen bubbles will expand in the tissues as pressure decreases. Different body parts can be affected, depending on where the bubbles are located. Medically Reviewed by a Doctor on 5/5/2016 Medical Author: Decompression Sickness (The Bends) Decompression Sickness (The Bends) 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% Decompression sickness | definition of decompression sickness by Medical dictionary Decompression sickness | definition of decompression sickness by Medical dictionary Definition Decompression sickness (DCS) is a dangerous and occasionally lethal condition caused by nitrogen bubbles that form in the blood and other tissues of scuba divers who surface too quickly. Description According to the Divers Alert Network (DAN), a worldwide organization devoted to safe-diving research and promotion, less than 1% of divers fall victim to DCS or the rarer bubble problem called gas embolism , air embolism , or arterial gas embolism (AGE). A study of the United States military community in Okinawa, where tens of thousands of sport and military dives are made each year, identified 84 DCS and 10 AGE cases in 1989–95, including nine deaths. This translated into estimates of one case in every 7,400 dives and one death in every 76,900 dives.

DCS symptoms can be quite mild, however, and many cases certainly go unnoticed by divers. At times the terminology adopted by writers on DCS can be confusing. Some substitute the term decompression illness (DCI) for DCS. Others treat DCI as a label encompassing both DCS and AGE. An older term for DCS is caisson disease, coined in the nineteenth century when it was discovered that bridge construction crews working at the bottom of lakes and rivers in large pressurized enclosures (caissons) were experiencing joint pain (a typical DCS symptom) on returning to the surface. Causes and symptoms The air we breathe is mostly a mixture of two gases, nitrogen (78%) and oxygen (21%). Unlike oxygen, nitrogen is a biologically inert gas, meaning that it is not metabolized (converted into other substances) by the body. For this reason, most of the nitrogen we inhale is expelled when we exhale, but some is dissolved into the blood and other tissues. During a dive, however, the lungs take in more nitrogen than usual.

This happens because the surrounding water pressure is greater than the air pressure at sea level (twice as great at 33 ft [10 m], for instance). As the water pressure increases, so does the pressure of the nitrogen in the compressed air inhaled by the diver. Because increased pressure causes an increase in gas density, the diver takes in more nitrogen with each breath than he or she would at sea level. Instead of being exhaled, however, the extra nitrogen safely dissolves into the tissues, where it remains until the diver begins his or her return to the surface (under some circumstances the extra nitrogen can cause nitrogen narcosis, but that condition is distinct from DCS). On the way up, decompression occurs (in other words, the water pressure drops), and with the change in pressure, the extra nitrogen gradually diffuses out of the tissues and is delivered by the bloodstream to the lungs, which expel it from the body. If the diver surfaces too quickly, however, potentially dangerous nitrogen bubbles can form in the tissues and cause DCS. These bubbles can compress nerves, obstruct arteries, veins, and lymphatic vessels, and trigger harmful chemical reactions in the blood. The precise reasons for bubble formation remain unclear.

How much extra nitrogen enters the tissues varies with the dive's depth and duration. Dive tables prepared by the U.S. Navy and other organizations specify how long most divers can safely remain at a particular depth. If the dive table limits are exceeded, the diver must pause on the way up to allow the nitrogen to diffuse into the bloodstream without forming bubbles; these pauses are called decompression stops, and are carefully calibrated. DCS can occur, however, even when a diver obeys safe diving rules. In such cases, the predisposing factors include fatigue , obesity, dehydration, hypothermia, and recent alcohol use. People who fly or travel to high-altitude locations without letting 12-24 hours pass after their last dive are at risk for DCS as well because their bodies undergo further decompression. This is true even when flying in commercial aircraft. Many travelers are unaware that to save money on fuel the cabin pressure in commercial aircraft is set much lower than the pressure at sea level.

At 30,000 ft (9,144 m), for instance, cabin pressure is usually equivalent to the pressure at 7,000-8,000 ft (2,133-2,438 m) above sea level, a safe setting for everyone but recent divers. Exactly how long a diver should wait before flying or traveling to a high-altitude location depends on how much diving he or she has done and other considerations. If there is uncertainty about the appropriate waiting period, the sensible course of action is to let the full 24 hours pass. Because the nitrogen bubbles that cause DCS can affect any of the body's tissues, including the blood, bones, nerves, and muscles, many kinds of symptoms are possible. Symptoms can appear minutes after a diver surfaces, and in about 80% of cases do so within eight hours. Pain is often the only symptom; this is sometimes called the bends, although many people incorrectly use that term as a synonym for DCS itself. The pain, which ranges from mild to severe, is usually limited to the joints, but can be felt anywhere.

Severe itching (pruritis), skin rashes , and skin mottling (cutis marmorata) are other possible symptoms. All of these are sometimes classified as manifestations of type 1 or "mild" DCS. Type 2 or "serious" DCS can lead, among other things, to paralysis , brain damage, heart attacks, and death. Many DCS victims, however, experience both type 1 and type 2 symptoms. Diagnosis Diagnosis requires taking a medical history (questioning the patient about his or her health and recent activities) and conducting a physical examination. Treatment DCS is treated by giving the patient oxygen and placing him or her in a hyperbaric chamber, an enclosure in which the air pressure is first gradually increased and then gradually decreased. This shrinks the bubbles and allows the nitrogen to safely diffuse out of the tissues. Hyperbaric chamber facilities exist throughout the United States. No matter how mild one's symptoms may appear, immediate transportation to a facility is essential. Treatment is necessary even if the symptoms clear up before the facility is reached, because bubbles may still be in the bloodstream and pose a threat.

DAN maintains a list of facilities and a 24-hour hotline that can provide advice on handling DCS and other diving emergencies. Prognosis DCS sufferers who undergo chamber treatment within a few hours of symptom onset usually enjoy a full recovery. If treatment is delayed the consequences are less predictable, although many people have been helped even after several days have passed. A 1992 DAN report on diving accidents indicated that full recovery following chamber treatment was immediate for about 50% of divers. Some people, however, suffer numbness, tingling, or other symptoms that last weeks, months, or even a lifetime. In the Okinawa study, six of the 94 patients experienced "long-lasting" symptoms even after repeated chamber treatments. Key terms Gas embolism — The presence of a gas bubble in the bloodstream that obstructs circulation. Hyperbaric chamber — A sealed compartment in which air pressure is gradually increased and then gradually decreased, allowing nitrogen bubbles to shrink and the nitrogen to safely diffuse out of body tissue. Lymphatic vessels — Vessels that carry a fluid called lymph from the tissues to the bloodstream.

Nitrogen narcosis — Also called "rapture of the deep," the condition is caused by increased nitrogen pressure at depth and is characterized by symptoms similar to alcohol intoxication. Prevention The obvious way to minimize the risk of falling victim to DCS is to follow the rules on safe diving and air travel after a dive. People who are obese, suffer from lung or heart problems, or are otherwise in poor health should not dive. And because the effect of nitrogen diffusion on the fetus remains unknown, diving while pregnant is not recommended. Resources [de″kom-presh´un] return to normal environmental pressure after exposure to greatly increased pressure. cerebral decompression removal of a flap of the skull and incision of the dura mater for relief of intracranial pressure. decompression sickness a condition resulting from a too-rapid decrease in atmospheric pressure, as when a deep-sea diver is brought too hastily to the surface. The popular term bends is derived from the bodily contortions its victims undergo when atmospheric pressure is abruptly changed from a high pressure to a relatively lower one. Called also caisson disease and divers' paralysis . A similar condition, altitude sickness , is suffered by aviators who ascend too rapidly to high altitudes.

Decompression sickness may also be a complication in a type of oxygen therapy called hyperbaric oxygenation , in which the patient is placed in a high-pressure chamber to increase the oxygen content of the blood. Personnel and the patient within the chamber must be protected from decompression sickness when they emerge from the high-pressure chamber. Cause. The phenomenon of decompression sickness is explained in terms of a law of physics: The greater the atmospheric pressure, the greater the amount of gas that can be dissolved in a liquid. The gas involved in this condition is the air we breathe, composed chiefly of nitrogen and oxygen. Under normal atmospheric pressure, nitrogen is present in the blood in dissolved form. If the atmospheric pressure is substantially increased, a proportionately greater amount of nitrogen will be dissolved in the blood. The same is true of oxygen, and this is the basis for hyperbaric oxygenation in the treatment of oxygen deficiency. The increase in pressure causes no ill effects. Nor will there be any ill effects if the pressure is gradually brought back to normal. When the decrease in pressure is slow, the nitrogen escapes safely from the blood as it passes through the lungs to be exhaled.

If the pressure drops abruptly back to normal, the nitrogen is suddenly released from its state of solution in the blood and forms bubbles. Although the body is now under normal air pressure, expanding bubbles of nitrogen are present in the circulation and force their way into the capillaries, blocking the normal passage of the blood. This blockage (or air embolus) starves cells dependent on a constant supply of oxygen and other blood nutrients. Some of these cells may be nerve cells located in the limbs or in the spinal cord. When they are deprived of blood, an attack of decompression sickness occurs. The oxygen in the blood reacts similarly when abnormal pressure is abruptly relieved. But because oxygen is dissolved more easily than nitrogen, and because some of the oxygen combines chemically with hemoglobin, the oxygen released in decompression forms fewer bubbles, and is therefore less troublesome. Symptoms and Treatment. Symptoms include joint pain, dizziness, staggering, visual disturbances, dyspnea, and itching of the skin. Partial paralysis occurs in severe cases; collapse and insensibility are also possible. Only rarely is decompression sickness itself fatal, although a diver while in this condition may suffer a fatal accident unless he or she is rescued.

Treatment consists of placing the victim in a decompression chamber where the air pressure is at the original higher level of pressure. If the victim is a diver, this is the pressure at the depth where he or she was working. Pressure in the chamber is then reduced to normal at a safe rate. de·com·pres·sion sick·ness a symptom complex caused by the escape from solution in the body fluids of nitrogen bubbles absorbed originally at high atmospheric pressure, as a result of abrupt reduction in atmospheric pressure (either rapid ascent to high altitude or return from a compressed-air environment); it is characterized by headache; pain in the arms, legs, joints, and epigastrium; itching of the skin; vertigo; dyspnea; coughing; choking; vomiting; weakness (and sometimes) paralysis; and severe peripheral circulatory collapse. Bone infarcts can occur from bubbles in nutrient vessels leading to long-term consequences. decompression sickness n. A disorder caused by the formation of nitrogen bubbles in the blood and tissues following a sudden drop in the surrounding pressure and characterized by joint pain, skin irritation, cramps, numbness, and, in severe cases, paralysis. It occurs especially in deep-sea divers when ascending rapidly from a dive.

Decompression sickness is often called "the bends." decompression sickness a painful, sometimes fatal syndrome caused by the formation of nitrogen bubbles in the tissues of divers, caisson workers, and aviators who move too rapidly from environments of higher to those of lower atmospheric pressures. Nitrogen breathed in air under pressure dissolves in tissue fluids. When ambient pressure is reduced too rapidly, nitrogen goes out of solution faster than it can be circulated to the lungs for expiration. Gaseous nitrogen then accumulates in the joint spaces and peripheral circulation, impairing tissue oxygenation. Disorientation, severe pain, and syncope follow. Treatment entails rapid return of the patient to an environment of higher pressure (hyperbaric therapy) followed by gradual decompression. Death is more often caused by drowning during syncope than by decompression sickness itself. Also called bends , caisson disease , diver's palsy, diver's paralysis. Compare barotrauma . bends A clinical complex caused by rapid whole-body decompression, with acute intravascular “boiling” of nitrogen and resultant morbidity (and mortality) in scuba divers and high-altitude pilots or workers in high-pressure environments (e.g., caissons) in chronic decompression sickness.

Clinical findings Headache, nausea, vomiting, vertigo, tinnitus, dyspnoea, tachypnoea, joint and abdominal pain; nitrogen gas in the brain causes air bubbles in meningeal vessels separating the blood “column”, convulsions, shock and possibly death. decompression sickness Emergency medicine A condition caused by rapid whole body decompression, with intravascular 'boiling' of nitrogen, and resultant morbidity or mortality; DS occurs in scuba divers and high-altitude pilots or workers in high-pressure environments Clinical, acute The 'bends' headache, N&V, vertigo, tinnitus, dyspnea, tachypnea, convulsions, shock, pain in joints and limbs–the bends, chest–the chokes and abdomen; nitrogen gas in brain causes 'boxcar' air bubbles in leptomeningeal vessels, which separates the blood 'column' and may cause death Clinical, chronic Caisson disease Dysbaric–ischemic–osteonecrosis with medullary infarcts of the femoral and humoral heads and rarely, malignancy—malignant fibrous histiocytoma, arising in bone infarction Management Hyperbaric oxygen.

See Hyperbaric oxygen therapy . de·com·pres·sion sick·ness (dē-kŏm-presh'ŭn sik'nĕs) A symptom complex caused by the escape from solution in the body fluids of nitrogen bubbles absorbed originally at high atmospheric pressure, as a result of abrupt reduction in atmospheric pressure (either rapid ascent to high altitude or return from a compressed-air environment); it is characterized by headache; pain in the arms, legs, joints, and epigastrium; itching of the skin; vertigo; dyspnea; coughing; choking; vomiting; weakness; possible paralysis; and severe peripheral circulatory collapse. Decompression Sickness - Causes, Types, and Symptoms Causes, Types, and Symptoms Guest Authors Also known as The Bends and Caisson Disease, Decompression Sickness is an illness that can affect divers or other people (such as miners) who are in a situation that involves pressure rapidly decreasing around the body. DCS, as it is commonly know, is caused by a build up of nitrogen bubbles in the body. When we breathe, approximately 79 of the air we're breathing is nitrogen.

As we descend in water, the pressure around our bodies increases, causing nitrogen to be absorbed into our body tissues. This is not actually harmful and it's quite possible for the body to continue to absorb nitrogen until it reaches a point called saturation, which is the point at which the pressure in the tissues equals the surrounding pressure. The problem arises when this pressure needs to be released. In order to release the nitrogen slowly from the body, a diver must ascend slowly and carry out decompression stops if necessary - this allows the nitrogen to slowly seep out of the body tissues and either immediately revert to being a gas or to become tiny harmless bubbles which will eventually become revert to gas. continue reading below our video LeBron vs. Michael: Who's Better? This process is called "Off-gassing" and is normally carried out through the lungs. If a diver ascends too fast and the nitrogen escapes the body tissue too quickly it becomes bubbles in the body and this leads to Decompression Sickness. The bubbles must normally be on the arterial side of the circulatory system to be harmful - they are usually harmless on the venous side.

There are several types of Decompression Sickness: Type I Decompression Sickness Type I Decompression Sickness is the least serious form of Decompression Sickness. It normally involves only pain in the body and is not immediately life threatening. It is important to note that symptoms of Type I Decompression Sickness may be warning signs of more serious problems. This is when the nitrogen bubbles come out of solution in skin capillaries . This normally results in a red rash, often on the shoulders and chest. Joint and Limb Pain Decompression Sickness This type is characterized by aching in the joints. It is not known exactly what causes the pain as bubbles in the joint would not have this effect. The common theory is that it is caused by the bubbles aggravating bone marrow, tendons, and joints. The pain can be in one place or it can move around the joint. It is unusual for bisymmetrical symptoms to occur. Type II Decompression Sickness Type II Decompression Sickness is the most serious and can be immediately life-threatening. The main effect is on the nervous system. Neurological Decompression Sickness When nitrogen bubbles affect the nervous system they can cause problems throughout the body.

This type of Decompression Sickness normally shows as tingling, numbness, respiratory problems, and unconsciousness. Symptoms can spread quickly and if left untreated can lead to paralysis or even death. Pulmonary Decompression Sickness This is a rare form of Decompression Sickness that occurs when bubbles form in lung capillaries. Fortunately, the majority of the time bubbles dissolve naturally through the lungs. However, it is possible for them to interrupt blood flow to the lungs which can lead to serious and life-threatening respiratory and heart problems. Cerebral Decompression Sickness It is possible for bubbles that make their way into the arterial blood stream to move to the brain and to cause an arterial gas embolism . This is extremely dangerous and can be identified by symptoms such as blurred vision, headaches, confusion, and unconsciousness. Other Forms of Decompression Sickness Extreme tiredness is very common in cases of Decompression Sickness and can sometimes be the only symptom of Decompression Sickness present. It is not know what causes this but you should be aware that extreme fatigue could be a sign of more serious problems. It is also possible for Decompression Sickness to occur in the inner-ear.

This is caused by bubbles forming in the cochlea 's perilymph during decompression. The result can be hearing loss, dizziness, ringing of the ears, and vertigo . Symptoms Decompression Sickness can manifest itself in many different ways and has many different symptoms, but the most common symptoms are: Extreme Fatigue Decompression Sickness - Injuries and Poisoning - Merck Manuals Consumer Version Double vision Loss of consciousness is rare. Symptoms of inner ear involvement, such as severe vertigo, ringing in the ears, and hearing loss, occur when the nerves of the inner ear are affected. Symptoms of lung involvement caused by gas bubbles that travel through the veins to the lungs, produce cough, chest pain, and progressively worsening difficulty breathing (the chokes). Severe cases, which are rare, may result in shock and death. Late effects of decompression sickness Dysbaric osteonecrosis (sometimes called avascular bone necrosis) is a late effect of decompression sickness that involves the destruction of bone tissue, especially in the shoulder and hip. Dysbaric osteonecrosis produces persistent pain and severe disability.

These injuries do not occur among recreational divers but, rather, among people who work in a compressed-air environment and divers who work in underwater habitats. These workers are exposed to high pressure for prolonged periods and may have an undetected case of the bends. Technical divers, who dive to greater depths than recreational divers, may be at higher risk than recreational divers. Bone and joint injuries may gradually progress over months or years to severe, disabling arthritis. By the time severe joint damage has occurred, the only treatment may be joint replacement. Permanent neurologic problems, such as partial paralysis, usually result from delayed or inadequate treatment of spinal cord symptoms. However, sometimes the damage is too severe to correct, even with appropriate treatment. Repeated treatments with oxygen in a high-pressure chamber seem to help some people recover from spinal cord damage. Diagnosis A doctor's evaluation Doctors recognize decompression sickness by the nature of the symptoms and their onset in relation to diving. Tests such as computed tomography (CT) or magnetic resonance imaging (MRI) sometimes show brain or spinal cord abnormalities but are not reliable. However, recompression therapy is begun before the results of a CT or MRI scan are available, except in cases in which the diagnosis is uncertain or the diver’s condition is stable.

X-rays are needed to diagnose dysbaric osteonecrosis. Prevention Divers can usually prevent decompression sickness by restricting the total amount of gas the body absorbs. The amount can be restricted by limiting the depth and duration of dives to a range that does not need decompression stops during ascent (called no-stop limits by divers) or by ascending with decompression stops as specified in authoritative guidelines, such as the decompression table in Diagnosis and Treatment of Decompression Sickness and Arterial Gas Embolism, a chapter in the United States Navy Diving Manual. The table provides a schedule for ascent that usually allows excess nitrogen to escape without causing harm. Many divers wear a portable dive computer that continually tracks the diver’s depth and time at depth. The computer calculates the decompression schedule for a safe return to the surface and indicates when decompression stops are needed. In addition to following a table or computer guidelines for ascent, many divers make a safety stop of a few minutes at about 15 feet (4.5 meters) below the surface. Following these procedures, however, does not eliminate the risk of decompression sickness.

A small number of cases of decompression sickness develop after no-stop dives, and the incidence of decompression sickness has not declined despite the widespread use of dive computers. The inability to eliminate decompression sickness may be because the published tables and computer programs do not completely account for the variation in risk factors among different divers or because some people fail to obey the recommendations of the tables or computer. Other precautions also are necessary: After several days of diving, a period of 12 to 24 hours at the surface is commonly recommended before flying or going to a higher altitude. People who have completely recovered from mild decompression sickness should refrain from diving for at least 2 weeks. People who have developed decompression sickness despite following dive table or computer recommendations should return to diving only after a thorough medical evaluation for underlying risk factors, such as a heart defect. Treatment Decompression Sickness Decompression Sickness Ernest S Campbell, MD, FACS First described in 1841, decompression sickness has gradually become better understood. Sport divers have provided a large body of material to study causing us to be able to learn more about the illness.

It's safe to say that DCS is caused by the production of nitrogen bubbles in the circulation, and this is related to the depthand time of a dive and to rate at which the diver ascends from depth. DCS and AGE combined form what is known as "decompression illness". Called "bends" by early investigators, it is now classically divided into Type I, Type II and "Type III" (a phrase coined by Bove and Neumann to describe a combination of DCS and arterial gas embolism). Type I DCS includes cutaneous manifestations and minor joint pain, or "pain only"; Type II includes severe symptoms related to the cardiopulmonary and neurological systems. Type III is a combination of AGE and DCS with neurologic symptoms. Pain syndromes spot the pain in the limbs-not the central skeleton. It is dull, difficult to characterize and localize and is located in the shoulders, elbows and hands in divers. Compressed air workers have more pain in their lower extremities. It is caused by bubbles, intravascular and extravascular with large gas stores in the fatty bone marrow. This is a cause of dysbaric osteonecrosis.

Neurologic Syndromes are increasing in sport divers and the spinal cord is the most commonly involved site. Symptoms include abdominal, low back, lower extremity pain, weakness and loss of feeling and function. Cerebral involvement is much more common than previously thought and may account for a portion of the "spinal cord" lesions. Peripheral nerves can also be involved causing numbness, limb pains and weakness. Early Treatment Recognition *Symptoms usually appear 15 minutes to 12 hours after surfacing* Signs Pain, arms, legs or trunk Dizziness Decompression sickness | Define Decompression sickness at Dictionary.com decompression sickness British Dictionary definitions for decompression sickness Expand noun 1. a disorder characterized by severe pain in muscles and joints, cramp, and difficulty in breathing, caused by a sudden and sustained decrease in air pressure, resulting in the deposition of nitrogen bubbles in the tissues Also called caisson disease, aeroembolism Nontechnical name the bends Collins English Dictionary - Complete & Unabridged 2012 Digital Edition © William Collins Sons & Co. Ltd.

1979, 1986 © HarperCollins Publishers 1998, 2000, 2003, 2005, 2006, 2007, 2009, 2012 Expand decompression sickness n. A disorder, seen especially in deep-sea divers or in caisson and tunnel workers, caused by the formation of nitrogen bubbles in the blood following a rapid drop in pressure and characterized by severe pains in the joints and chest, skin irritation, cramps, and paralysis. Also called aeroemphysema, bends, caisson disease. The American Heritage® Stedman's Medical Dictionary Copyright © 2002, 2001, 1995 by Houghton Mifflin Company. Published by Houghton Mifflin Company. Expand decompression sickness A common disorder that affects deep-sea divers following a sudden drop in the surrounding pressure, as when ascending rapidly from a dive. When divers are underwater, the amounts of gases such as O2, CO2, and N2 in their blood increase due to the increased pressure.

As they ascend to the surface and the pressure decreases, the gases in their blood expand. The extra oxygen is absorbed by the body; the extra CO2 is excreted efficiently; but nitrogen, which the body does not use, forms bubbles in the blood and tissues. These bubbles cause severe pains in the joints and chest, skin irritation, cramps, and possibly paralysis. Decompression sickness can be avoided by ascending slowly to the surface, or by spending time in a decompression chamber. The American Heritage® Science Dictionary Copyright © 2002. Published by Houghton Mifflin. All rights reserved. People invent new words all the time, but which ones actually make it? Word of the Day

Question: What is Decompression Sickness commonly called?
Answer: The Bends