In decompression sickness the manifestations are due to formation of nitrogen bubbles in body tissues and fluids. On exposure to lower atmospheric pressure the partial pressure of nitrogen dissolved in body fluids and tissues exceeds nitrogen partial pressure in the lungs. If this pressure reaches the point where nitrogen evolves from tissues and fluids faster than it can be transported by blood to the alveolar membrane to diffuse into alveolar air, bubbles will form.
Bubbles large enough to produce symptoms develop when the partial pressure of nitrogen in tissues rapidly becomes more than twice as great as nitrogen partial pressure in the atmosphere. This situation can arise in a diver whose tissues are saturated with nitrogen at a depth somewhat in excess of 33 feet who surfaces rapidly, or by a flier who rapidly ascends from sea level to higher than 18,000 feet.
In keeping with Henry’s law. gases in contact with liquids dissolve in direct proportion to their partial pressures. The processes of nitrogen diffusion and transport necessary for equilibration between tissues and alveolar air require time. Since nitrogen must be transported by blood, equilibration in highly vascular tissues occurs more rapidly than in those that are poorly vascularized. Fatty tissue is not only poorly vascularized but in addition takes up larger volumes of nitrogen since nitrogen is far more soluble in lipids than in water.
Facts You Must Know About Decompression Sickness
The complete elimination of excess nitrogen from the body after exposure to a lower partial pressure of nitrogen in the atmosphere requires about 12 hours. About 75 per cent of the total is eliminated within 2Va hours, mainly from aqueous solution in plasma and interstitial tissue. The slower component arises mainly from tissues high in lipid content such as fat deposits, bone marrow, and spinal cord.
The total amount and the rate at which nitrogen is taken into solution during a dive will depend not only upon the depth but the time spent at depth. The magnitude of this depth-time factor and the rate of ascent determine whether decompression sickness occurs. Beyond certain depth timeless, it is necessary to ascend in stages with time to allow an adequate amount of denitrogenation to occur before ascending further. Stage decompression 15 cased on never exceeding the 2:1 ratio of alveolar :: tissue partial pressure of nitrogen. These general principles also apply in altitude decompression sickness, in which tissues are saturated at 1 atmosphere when ascent begins.
The symptoms produced depend primarily upon the site of bubble formation. The size of the bubbles and their rate of growth influence the severity of symptoms. Although bizarre dinical pictures may occur, certain patterns frequently, suggesting a predilection to bubble formation in some tissues and organs. The most common and familiar manifestation is *bends.” This consists of deep, boring, and usually constant pain in the vicinity of large Jffi imts. the knees and shoulders being most frequently involved.
Pain may be so severe as to be incapacitating. Most cases of bends occur within the first 30 minutes after decompression, that is, after reaching a critical altitude or after surfacing following .dive in which the depth-time factor was exceeded. Bends in flight disappear completely during descent.
Subjective skin manifestations, usually prickling or burning sensations, termed the “itches” or ”creeps,” occur rather commonly in fliers. Although objective skin manifestations occur uncommonly, a characteristic pale, cyanotic mottling of the skin sometimes appears, usually over the upper trunk and typically ’ater than bends.
Chokes, believed due to bubbles in the pulmonary vasculature, occurs later than bends, and consists of burning retrosternal distress and cough. Relieved at first by shallow breathing, the symptoms progress in severity until coughing becomes paroxysmal and uncontrollable. Recompression by descent produces partial relief, but symptoms may persist for several days. Often associated with cyanosis and syncope, the syndrome has ominous significance because shock and coma may ensue.
Homonymous scintillating scotomas are neurologic manifestations of decompression sickness. Although apparently not observed in divers, they are common manifestations at high altitude. They are transient, and frequently disappear while still at altitude.
One or more of the manifestations already mentioned usually precede more serious stages of decompression sickness, which are characterized by neurologic manifestations and sometimes vasomotor instability that may progress to circulatory collapse with cyanosis, shock, and coma. Almost every possible neurologic sign has been observed, including motor paralysis.
In altitude decompression sickness, neurologic findings are usually limited to transient paresis and dysesthesias. The lower segments of the spinal cord are most frequently involved in divers, and permanent residuals may occur. In altitude decompression sickness a period of apparent recovery from the earlier manifestations may precede the appearance of circulatory collapse and shock. During this latent period vague symptoms can usually be elicited, and signs of instability of blood pressure and heart rate and at least minor focal neurologic signs can be detected. Hemoconcentration, with hematocrit as high as 60 to 70 per cent, is a characteristic finding that presumably results from widespread vascular injury and loss of plasma into tissues .
Treatment of Decompression Illness
All the varied manifestations of decompression sickness respond rapidly to early and adequate treatment by recompression. Descent from altitude produces sufficient recompression to abolish the early manifestations, but merely retards the appearance of the more slowly developing serious forms of decompression sickness.
In such cases widespread bubble formation has presumably already occurred, and descent is entirely analogous to inadequate recompression therapy during which symptoms subside only temporarily. The clinical picture of decompression sickness in divers and fliers might also be expected to differ because of the greater volumes of nitrogen that must be eliminated in divers on decompression.
Divers can prevent decompression sickness by knowing and following established limits for depth and time at depth. Limitations of air supply unfortunately often prevent ascent in stages after depth-time limits have been exceeded. Adequate denitrogenation by breathing 100 per cent oxygen prior to and during ascent is an effective preventive measure in fliers. Because inadequate cabin pressurization is rarely anticipated, the procedure is often neglected.
Divers should avoid the increased hazard of repeating a dive before adequate time at surface to eliminate excess nitrogen from the previous dive. Similarly, fliers who have experienced decompression symptoms during a flight should delay return to even relatively low altitudes because the expansion of bubbles still present in tissues may cause a rapid recurrence of more serious symptoms. The hazard of exposure to altitudes as low as 7000 feet after even safe depth-time dives should be recognized.