Complications From Expansion of Air in the Lungs During Ascent

2.2.2.2 Mediastinal Emphysema

Mediastinal emphysema is the result of air being forced into the tissues about the heart, the major blood vessels, and the trachea (windpipe) in the middle of the chest.

Gas trapped in the spaces between tissues may expand rapidly with continuing decompression, causing impaired venous return. The symptoms of mediastinal emphysema are pain under the sternum and, in extreme cases, shortness of breath or fainting due to interference with circulation as the result of direct pressure on the heart and large vessels. Treatment in mild cases of mediastinal emphysema is symptomatic. In more severe cases, oxygen inhalation may aid resolution of the trapped gas. For severe, massive mediastinal emphysema, recompression is required.

2.2.2.3 Subcutaneous Emphysema

Subcutaneous emphysema, which may be associated with mediastinal emphysema, is a result of air being forced into the tissues beneath the skin of the neck extending along the facial planes from the mediastinum. Unless it is extreme (characterized by a crackling of the skin), the only symptoms of subcutaneous emphysema are a feeling of fullness in the neck and a change in the sound of the voice. Oxygen breathing will accelerate the absorption of this subcutaneous air.

2.2.2.4 Gas Embolism

The most serious result of pulmonary overpressurization is the dispersion of alveolar gas into the pulmonary venous system. The gas is carried to the heart, and then into the systemic circulation, resulting in gas emboli in the coronary, cerebral, and other systemic arterioles. Gas bubbles continue to expand with further decrease of pressure, increasing the severity of clinical signs.

The clinical features of traumatic arterial gas embolism may occur suddenly or be preceded by dizziness, headache, or great anxiety. Unconsciousness, cyanosis, shock, and convulsions follow quickly. The convulsions may be severe and recurrent, and may require heavy sedation. Motor and sensory deficits occur in various degrees and distribution. Death results from coronary or cerebral occulsion with cardiac arrhythmia, respiratory failure, circulatory collapse, and shock. Physical

examination may reveal (1) air bubbles in the retinal vessels of the eye; (2) Liebermeister's sign (a sharply defined area of pallor in the tongue); (3) marbling of the skin; (4) hemoptysis; (5) focal or generalized convulsions; or (6) other neurological abnormalities. A chest cold or bronchitis can cause problems resulting from coughing, increased breathing resistance in airways, and the risk of gas embolism resulting from temporary obstruction of an air passage. Diving with a chest cold or bronchitis should be avoided.

The only effective treatment of gas embolism is recompression to reduce the size of the bubbles, force them into solution, and thus restore effective circulation. A recompression chamber is required. Treatment prior to recompression is merely symptomatic. A patient should be kept in the head-down position, which may help to keep bubbles from reaching the brain. Placing the patient on the left side helps to maintain cardiac output, which may be impaired because the large amount of air has decreased the efficiency of the pumping action of the heart. In nonfatal cases, residual paralysis, myocardial necrosis, and other ischemic injuries may occur if recompression is not immediately carried out, and may occur in adequately treated patients if there is a delay in initiating therapy. Although most surgical and medical therapeutic pressure facilities will operate at 2 to 3 atmospheres absolute, they must have the capacity to reach 6 atmospheres absolute safely. Central nervous system decompression sickness is clinically similar to gas embolism and the treatment for both requires a recompression chamber. Treatment such as oxygen inhalation, body positioning (head-down 15 degree angle), and hypothermia are only partially effective without recompression. However, these steps must be taken until a recompression chamber can be reached (See Paragraph 16.3.4).

2.2.2.5 Overexpansion of the Stomach and Intestine

In the stomach and large intestine there is ordinarily a liter or more of gas entrapped. Since the intestines are surrounded by soft tissues, the compression and reexpansion of these air bubbles is ordinarily not noticeable and carries no special hazard. If, while diving, one tends to swallow air, it may be necessary to expel gas by belching or by passing gas per rectum, in the course of ascent. For the same reason, eating large amounts of gas producing foods prior to diving is not recommended.

An excess of gas in the stomach or intestine during ascent may cause marked discomfort and vasovagal effects. In an extreme case, breathing difficulty may be experienced. The causes of air swallowing, such as chewing gum during pressure exposure, should be avoided.

2.2.3 Indirect Effects of Pressure

The indirect effects of pressure result from changes in the partial pressures of the gases in the breathing medium. The mechanism of these effects include saturation and desaturation of body tissues with dissolved gas, and changes of body functions by abnormal gas tensions.

2.2.3.1 Nitrogen Absorption and Elimination

At sea level the body tissues are equilibrated with dissolved nitrogen equal to the partial pressure of nitrogen in the lungs. Upon exposure to altitude or pressure, the partial pressure of nitrogen in the lungs will change and the tissues will either lose or gain nitrogen to reach a new equilibrium with the nitrogen pressure in the lungs. Taking up nitrogen in tissues is called absorption or uptake. Giving up nitrogen from tissues is termed elimination. In air diving, nitrogen absorption occurs when a diver is exposed to an increased nitrogen partial pressure. Elimination occurs when pressure decreases. This is true for any inert gas breathed.

The process of absorption consists of several phases, which include transfer of inert gas from the lungs to the blood, then from the blood to the various tissues through which it flows. The gradient for gas transfer is the partial pressure difference of the gas between the lungs and blood and the blood and the tissues. The volume of blood flowing through tissues is usually small compared to the mass of the tissue, but over a period of time the gas delivered to the tissue will cause it to become equilibrated with that carried in solution in the blood. The rate of equilibration with the blood gas depends upon the volume of blood flow and the respective capacities. of blood and tissues to absorb dissolved gas. For example, fatty tissues hold significantly more gas than watery tissues and will thus take longer to absorb or eliminate excess inert gas.

The process of elimination is the reverse of absorption. During ascent, and after surfacing, the tissues lose excess inert gas to the circulating blood by diffusion, the gradient being the difference

between the inert gas partial pressure in each tissue and that in the blood vessels after the blood has equilibrated to the gas in the lungs. The amount of inert gas that can be taken up in the blood is limited, so the tissue inert gas tension falls gradually. As in absorption, the rate of blood flow and the amount of inert gas dissolved in the tissues and blood determine the rate of elimination. After decompressing to the surface or ascending to a shallower level, elimination at the new level may require 24 hours or

more.

During decompression, the blood and tissues can hold gas in supersaturated solution to some degree, without bubbles being formed. A supersaturated solution is one in which the blood and tissues hold more gas than is possible at equilibrium at the particular temperature and pressure. Because of the ability of the blood and tissue to become supersaturated for short periods of time, a diver can ascend at least part of the way regardless of the depth and duration of his dive. An outward gradient is established and inert gas is eliminated from body tissues. This permits the diver to ascend further after some period of time. The process is continued until a diver can reach the surface. The diver's body will still contain inert gas in supersaturated solution in some tissues, but this is normally safe if kept within proper decompression limits, and if further pressure reduction such as ascending to altitude does not take place (See Paragraph 6.4).

The basic principles of absorption and elimination of gas are the same for any inert gas breathed. Differences exist in the solubility and rates of diffusion of gases in water and fat. Helium is much less soluble in tissues than is nitrogen and diffuses faster. Thus, helium saturation may occur somewhat more rapidly than for nitrogen. It would appear that the more rapid saturation and desaturation that occurs with helium could require less decompression after long deep dives than when air is breathed. However, somewhat deeper decompression stops are required with helium to prevent it from coming out of solution as bubbles. As a result, some of this advantage is lost. The greatest advantage in the use of helium-oxygen mixtures is the freedom from narcosis and the decrease in breathing resistance, rather than a decompression advantage.

2.2.3.2 Decompression Sickness

If the elimination of gas by blood flowing through the lungs is inadequate to parallel the rate of reduc

tion of external pressure, the amount of supersaturation of gas in the tissues may permit the gas to come out of solution in the form of bubbles. Bubbles forming in the blood stream will block circulation, while bubbles in tissues will distort the tissues as the bubbles expand. Symptoms occurring depend on the location of the bubbles, whether in joints, muscles, bones or nerves. When the brain is affected, dizziness, deafness, paralysis and unconsciousness can occur. Bubbles in the spinal cord can cause paralysis and loss of feeling in parts of the body affected. Bubbles in respiratory systems cause choking and asphyxia. Skin bubbles produce itching and rash. Involvement of the brain and spinal cord can cause severe disabilities that can threaten the life of a diver if treatment is not initiated promptly. Treatment of decompression sickness consists of recompressing the diver to a depth sufficient to cause the bubbles to return to solution. When symptoms and signs are cleared, careful decompression to the surface again should follow, so that bubbles do not again form (See Paragraph 16.3.1).

Prevention of decompression sickness can usually be accomplished by adhering to the proper decompression table. Even though the correct decompression procedure is followed, cases of decompression sickness sometimes occur. Factors which may increase the likelihood of decompression sickness even when proper tables are used include excessive obesity, loss of sleep, fatigue, use of alcohol and its aftereffect, dehydration, various illnesses, particularly those which affect the circulatory system, and anything that causes poor physical condition and poor circulation. Heavy exertion and cold during a dive also contribute to excess inert gas being absorbed and interferes with its elimination during decompression. Anything that impedes blood flow, such as a cramped position, interferes with inert gas being eliminated (U.S. Navy Diving Manual 1973). It is important to note that the significant individual differences which exist with respect to physical condition and the effects of environmental parameters, also play an important role in susceptibility to decompression sickness.

WARNING

Symptoms of Decoripression Sickness Can Occur as toms as 2! H. v 1.7ying a Dive.

A device known as a doppler bubble detector has demonstrated the ability to detect gas bubbles in

the blood stream and tissues. The device utilizes high frequency sound waves which, when passed through blood vessels or tissues, indicate when bubbles of gas are present by a noticeable change in the frequency of the sound emitted from the device. These devices are being used experimentally and show great promise for the future.

2.2.3.3 Aseptic Bone Necrosis (Dysbaric Osteonecrosis)

Aseptic bone necrosis refers to destructive changes in bone, in which the relative density of the affected bone is increased by sclerosis, as well as cystic changes. Neither of these are of infectious origin. These changes have been noted in many conditions such as chronic alcoholism, pancreatitis, sickle-cell anemia, during the use of systemic steroids, and in caisson workers and divers. The development of changes in the hips and shoulder joints of caisson workers with crippling effects from joint breakdown was first noted in 1888, but the disease has not had much attention in divers who generally observe more conservative decompression.

Many caisson workers experience a high incidence of bends as a result of inadequate decompression time. It is felt that some of the bubbles causing pain in joints may have lodged in the arteries that supply blood circulation to bone, blocking the flow of blood for a period of time. If the blockage and stagnation of blood flow lasts for 12 hours or more, the bone cells thus affected may die (Kindwall 1972). If the lesions occur in the head of bones as the femur or humerus, the weakened underlying bone that supports the cartilage covering the bone will collapse with weight-bearing and activity, causing the joint surface to break down and become irregular. Pain occurs with movement of these joints accompanied by muscle spasms around the joint and inability to use the joint in a normal manner.

Lesions also occur in the shafts of long bones, but these never cause symptoms or disability though the bony scars of increased density may appear on X-ray after deposition of the new bone occurs, with healing of the area. Few changes are seen in the knees and rarely in the elbows, wrists, or ankles (Kindwall 1972).

It appears that aseptic bone necrosis can occur after only one severe instance of decompression sickness, though a time period of months must elapse before evidence of bony change can be seen

by X-ray of the affected bones. Frequency of exposure to pressure, number of cases of bends, adequacy and promptness of recompression treatment, and the amount of pressure exposure have been listed as possible factors related to likelihood of developing bone lesions.

The cause of aseptic bone necrosis has still not been demonstrated beyond doubt. The highest incidence occurs in workers who have used inadequate decompression procedures or who have experienced bends on one or more occasions. There is some evidence that fat emboli may occlude circulation of blood vessels in bone and other tissues, and thus may be a factor in development of hip lesions in the chronic alcoholic with a fatty liver, or following pressure exposure in which bends occur.

In patients with gout, lesions of the hip joints have contained sodium urate crystals, which may have been a factor in the destruction of the joint surface. Lesions of bone in workers exposed to pressure may not become apparent on X-rays of the joints for 4 months to 5 years after the pressure exposure. *

A 3-year survey of 350 full-time divers in the British Navy tabulated a 5 percent incidence of aseptic bone necrosis, in which half of the affected divers had no evidence of decompression sickness while using Royal Navy decompression tables only.* The British Navy's decision has been not to permit divers with joint lesions to continue to dive.

2.2.3.4 Inert Gas Narcosis

Among the major factors likely to cause performance impairment in divers at increased ambient pressures is inert-gas narcosis. Although the common inert gases (nitrogen and helium) associated with diving are physiologically inert under normal conditions, they have distinct anesthetic properties when the partial pressure is sufficiently high. The problem of compressed air "intoxication" has long been recognized by divers and researchers.

There are several theories as to the basic cause of inert gas narcosis including: increased carbon dioxide tension; impairment of carbon dioxide diffusion in the alveoli; increased oxygen pressure and anxiety or claustrophobia. The divergent opinions as to the cause may to some extent be explained by the fact that, at raised barometric pressures there are simultaneous increases in alveolar oxygen pressure, alveolar nitrogen pressure, and gas density. Experiments where the subjects are exposed to "normal"

* Robert D. Workman, M.D., 1973; personal communication.

air at different barometric pressures will therefore not permit any differentiation between these factors as to their possible narcotic effects (Hesser 1963). In spite of such divergent opinions as to the basic cause, there seems to be no doubt that the anesthetic properties of high nitrogen pressure constitutes an important causative factor.

Narcosis is characterized by symptoms similar to alcohol intoxication. It becomes evident at a depth of about 100 feet. Beyond this depth, most compressed air divers show some impairment of thought, judgment, and the ability to perform tasks that require mental or motor skill. Such impairment, even if mild, obviously constitutes a potential hazard to the diver's safety. Most divers lose their effectiveness at about 200 feet, and at about 250 feet, the average diver will be unable to function well enough to ensure his own safety.

Like alcohol, the effects of nitrogen vary with the individual. By conscious effort, the hazards can be minimized within certain limits. The sequence of events for the average man under the influence of high-pressure nitrogen in a breathing medium of air is as follows:

cumstance causing retention of carbon dioxide. In the inexperienced diver, anxiety is likely to advance the onset of symptoms. However, experience, strong will, and frequent deep diving all help to increase the tolerance to high-nitrogen tensions. The principles of prevention lie in common sense and proper diving procedures.

To treat inert gas narcosis the diver simply ascends to shallower depths. Except for general tiredness, recovery is usually immediate and complete.

2.3 OXYGEN POISONING

Low-pressure oxygen poisoning can occur if more than 60 percent oxygen is breathed at 1 atmosphere of pressure for 12 hours or more. I ung irritation with coughing and painful breathing can develop (U.S. Navy Diving Manual 1973). A form of pneumonia, with lung damage, can develop if the exposure is continued. When oxygen is administered for long periods of time, sufficient dilution with air usually is done to prevent such occurrences. During long pressure chamber exposures, a diver may be exposed to a partial pressure greater than 0.6 atmospheres of oxygen for a sufficient time to produce lung irritation (U.S. Navy Diving-Gas Manual 1971). High-pressure oxygen poisoning can occur when divers are exposed to more than 1 atmosphere of oxygen for a period of minutes to hours. The lower the oxygen partial pressure, the longer the time before symptoms develop. Because it is the partial pressure of oxygen itself which causes toxicity, the problem can occur while breathing mixtures of oxygen with nitrogen or helium at depth. No time limitations apply if the partial pressure of the oxygen is maintained between 0.2 and 0.5 atmospheres (U.S. Navy Diving-Gas Manual 1971).

Other factors which may contribute to the onset of oxygen toxicity are: degree of exertion, amount of carbon dioxide inspired and retained; and basic individual differences in susceptibility.