The USN Treatment Tables

by John Zumrick

Though other procedures and methods have evolved, the U.S. Navy treatment tables have become a standard of reference for treating decompression illness. Here, naval medical officer, Dr. John Zumrick describes USN procedures and some of the history and thinking behind them.

For the technical diver, dives have become longer and deeper, with many approaching or exceeding the limits of traditional decompression tables. Tables used to manage these exposures are less thoroughly tested than those of more limited and, therefore, more common dives, so it is reasonable to expect the incidence of decompression illness (DCI) to be higher. Moreover, owing to variations in individual physiology, even commonly used decompression schedules are not entirely bends free. As a result, a technical diver runs a higher-than-normal chance of experiencing a case of DCI (Note that the overall estimated decompression risk for sport divers is about .02% or "one in 5000 dives," though the risk for extended range dives is probably higher. See "Decompression Safety," by Richard Vann, pg.13) .

Recompression therapy is the definitive treatment for DCI. Begun shortly after the onset of bends, recompression can result in dramatic, almost immediate improvement and cure, even while the diver is still being compressed to treatment depth. Delayed therapy, however, is far less successful in effecting a cure and may require multiple treatments.

Since the 19th century bubble formation has been implicated as the cause of decompression illness. DCI is caused by an excessively rapid lowering of ambient pressure. This reduction in pressure results in inert gas dissolved in tissue and blood coming out of solution and entering the gas phase, causing bubbles to form in tissue and blood. Signs and symptoms of bends can be grouped into two broad categories based upon their severity.

In traditional terminology, "pain only," or Type I, decompression sickness encompasses the relatively minor forms of the syndrome and includes limb pain, lymphatic manifestations and skin manifestations. Limb pain is the most common symptom of DCI, occurring in about 90% of USN cases. (Based on recent incident data from DAN and others, more than half the sport diving cases reported have neurological involvement&endash;ed). This pain involves the arms and shoulders in a majority of cases and varies in intensity from a mild, nearly imperceptible ache to steady, nearly unbearable pain. The exact mechanism by which bubbles cause this pain has not been determined, but it is thought that pain that responds to position is caused by local bubbles within the tendons and ligaments around joints, while deep boring pain that does not repond to movement, may be due to increased pressure in the longbones. Lymphatic manifestations are thought to caused by bubbles blocking lymph flow resulting in swelling. Skin manifestations can also ocurr, which include itching, rash and purple mottling, usually over the trunk and back.

Classical "Type II decompression sickness" is normally neurological, but does include "chokes" and extreme fatigue. Presenting signs and symptoms of these DCI manifestations are shown in Figure 1 below. The mechanisms by which bubbles produce the neurological manifestations are not well defined, either, though it is thought that bubbles trapped within and blocking pulmonary arteries may account for chokes.

Elliott and Hallenbeck have elucidated the mechanism of spinal cord decompression sickness in dogs. Normally, blood flow throughout the spinal cord and adjacent epidural vessels is slow but adequate. Increases in central venous pressure due to bubbles in the pulmonary artery contribute to reduction in blood flow through the spinal cord and epidural vessels. Bubbles may also form within these vessels, reducing blood flow. Blood-bubble interface may lead to platelet adhesion and the release of other chemical substances, which themselves may reduce blood flow. The resultant reduction in blood flow results in tissue hypoxia leading to paralysis. Thus, although DCI is initiated by the formation of inert gas bubbles, it is a manifestation of additional pathologic changes, particularly when not treated early.

Prior to 1937, the U.S. Navy utilized treatment Table 1, based on never allowing the inert gas tension in the body's slowest "tissue compartment" to exceed twice that of ambient pressure. In 1937, Yarborough and Behnke shortened Table1 by including oxygen breathing at a depth of 60 fsw (18 msw) or less. The Behnke Yarborough modification of Table 1 included recompression to 165 fsw (50 msw) for 30 minutes, followed by 90 minutes of breathing oxygen at 60 fsw (18 msw). The end result was a saving of 45% of decompression time from the original table.

In 1945, Van der Aue standardized recompression therapy in the U.S. Navy. His procedures formed the basis for treatment Tables 3 and 4 (Note that these tables are "still on the books" but are seldom used today due to their length, the operational difficulties involved, and their perceived ineffectiveness. See discussion below.&endash;ed.). The tables included initial recompression to 165 fsw (50 msw) for 30 to 120 minutes; an overnight soak on air at depths shallower than 60 fsw (18 msw) for 12 to 24 hours; and the use of 100% oxygen at 60 fsw (18 msw) or less. Unfortunately, operational use of these tables between 1946 and 1961 yielded a treatment failure rate of nearly 30%.

In 1965, Goodman and Workman proposed changes to these tables that formed the basis for the current oxygen treatment tables, Tables 5 and 6. They eliminated the initial recompression to 165 fsw (50 fsw) in cases of pure decompression sickness and lengthening of the oxygen breathing periods at 60 and 30 fsw (18 and 9 msw). Recompression to 165 fsw (50 msw) was reserved for cases of arterial gas embolism. The initial experience with these tables indicated a failure of less than 9%.

Current USN treatment methods incorporate two separate goals: 1) the immediate reduction in bubble size and 2) permanent bubble resolution.

Immediate recompression effects immediate reduction in bubble size, but the practical effect of this is limited. Assuming for the moment that gas bubbles are spherical, recompression to 66 fsw (20 msw) reduces a bubble to 1/3 of it's volume at sea level pressure, while recompression to165 fsw (50 msw) reduces it to 1/6 of it's original volume. Further recompression to 198 fsw (60 msw) reduces the bubble to only 1/7 of surface volume, an insignificant difference compared to its volume at 165 fsw (50 msw). Thus recompression deeper than 165 fsw or 50 msw is thought to be therapeutically insignificant, particularly when taking into account the effects of narcosis, addition gas loading, and the resulting extremely long decompression times.

Recompression produces an immediate reduction in bubble size favoring restoration of circulation and reduction of bubble effects in tissue. However, once this initial reduction in bubble size has been acheived, additional inert gas uptake by the bubbles may actually favor later bubble growth.

To promote bubble resolution, high partial pressures of oxygen are used. When 100% oxygen is breathed, blood inert gas tension is reduced to zero, creating a high gradient for the elimination of inert gas from bubbles and from the body. Recompression to only 60 fsw (18 msw) therefore produces two advantages. Recompression increases inert gas tension within the bubble, and oxygen breathing reduces the blood inert gas level thereby increasing the gradient and thus maximizing the elimination of inert gas and bubble resolution. Additionally, the body takes up no additional inert gas while oxygen breathing. This reduces required decompression time.

The above discussion assumes that bubble resolution occurs in a medium where tissue blood flow is fast, effectively carrying away the inert gas liberated from the bubble. However, in cases where tissue blood flow is reduced, such as spinal cord DCI, bubble resolution may be limited by the rate gas is carried away from the tissues by circulation rather than by gas diffusion from the bubble.

In addition to promoting more rapid bubble resolution, oxygen has other therapeutic advantages. Oxygen provides better tissue oxygenation to areas where blood flow may not be adequate, thereby reducing tissue injury. Finally, oxygen has been shown to have an anti-swelling effect on nervous tissue, which may be useful, particularly in cases of spinal cord DCI.

Treatment Tables

Though there are a variety of approachs and tables that are used successfully today by those involved in treating DCI, the U.S. Navy uses two types of treatment tables: 1) those using hyperbaric oxygen breathing in relatively short treatments 2) and those employing air breathing throughout treatments of relatively long duration (Note that with the advent of oxygen therapy, air treatments have "fallen out of favor" in the non-military community, and are viewed as not very effective in most instances&endash;ed.).

In most cases when oxygen is available, the oxygen breathing tables (Tables 5, 6, and 6A) are strictly preferred to the air-breathing tables (Table 4). The oxygen tables have several advantages. First, bubbles resolve more quickly during oxygen than air breathing. Second, hyperbaric oxygen reduces central nervous system edema. As a result, these tables are more effective in treating cases in which treatment has been delayed (A common in sport diving incidents&endash;ed.); whether this improvement is due to the anti-edema effect or to the improved tissue oxygenation is unclear. Oxygen-breathing tables are also shorter than traditional air tables. This gives patients who need other hospital care access to therapy that cannot be administered while in the chamber. Finally, the patient may be decompressed at any time from an oxygen table without worsening symptoms, because the tissue absorbs no additional inert gas during treatment.

Treatment Table 5, which was once described as a "carrot to lure the diver into the chamber" is intended for the treatment of pain-only DCI where symptoms completely resolve within 10 minutes at 60 fsw (18 msw); cases of omitted decompression; or as a test of pressure used to determine if atypical symptoms may be decompression illness. Many diving doctors in the U.S. today will not use a Table 5 for liability reasons related to the potential for undiagnosed neurological involvement or recurrence of symptoms, though others believe it works and should be used when appropriate. A profile of Table 5 is shown in the Figure 2 below.

Recompression is from the surface to 60 fsw (18 msw) at 25 fsw (8 msw) per minute, with the patient breathing oxygen throughout the descent. The patient continues to breath oxygen for 20 minutes at 60 fsw (18 msw). After the initial 20-minute oxygen breathing period, the patient breathes chamber air for five minutes followed by a second 20-minute period of oxygen breathing. The five-minute air breathing period reduces the potential for central nervous system (CNS) oxygen toxicity, usually manifested as a seizure. After the second oxygen breathing period, and if all symptoms have resolved within 10 minutes of arrival at 60 fsw (18 msw), the patient is decompressed at 1 foot per minute to 30 fsw (9 msw) while continuing to breathe oxygen. Upon arrival at 30 fsw (9 msw), the patient takes a five-minute air break, followed by a final 20-minute oxygen period at 30 fsw (9 msw). After a third five-minute air break, the patient is decompressed while breathing oxygen at 1 foot per minute to the surface. Total treatment time is 135 minutes.

Treatment Table 6 is used to treat acute neurological DCI and for all other circumstances where treatment according to Table 5 do not apply. Table 6 is similar in many respects to Table 5 but requires additional and extended oxygen breathing periods. As shown in the Figure 3, Table 6 requires three 20-minute oxygen breathing periods, called "cycles" at 60 fsw (18 msw) as compared to two required by Table 5. Additionally, two additional oxygen breathing periods interspersed with breathing chamber air can be added at 60 fsw (18 msw) in the event of incomplete resolution of symptoms during the initial treatment periods. Treatment Table 6 also differs from Table 5 in that two 60-minute oxygen breathing periods are required at 30 fsw (9 msw) with 15-minute air breathing breaks between oxygen breathing periods. Again, Table 6 can be extended at 30 fsw (18 msw) to allow the insertion of two more 60-minute oxygen breathing periods if necessary. Total treatment time is 285 minutes without table extensions.

Table 6 is replacing Table 5 as the preferred table for treating all forms of DCI. The extra oxygen breathing at depth minimizes the chance of symptoms recurring after treatment for all cases successfully treated. Moreover, this table provides more flexibility in dealing with difficult or slow-to-respond cases.

Treatment Table 6A is intended for the treatment of cerebral air embolism, though there is some question as to its usefulness when there have been major delays between the time of the incident and instituting treatment, and for treating neurological decompression illness. Table 6A (Figure 4) adds a rapid compression to 165 fsw (50 msw) for 30 minutes to a Table 6. The pressurization to 165 fsw (50 msw) provides additional bubble compression in an effort to reestablish circulation quickly to occluded vessels in the brain. If symptoms resolve within 30 minutes, the patient is decompressed to 60 fsw (18 msw), where treatment according to Table 6 is begun. If in the judgment of the treating physician additional treatment at 165 fsw (50 msw) is required, the patient can be held at the higher pressure for up to two hours and decompressed on treatment Table 4.

Treatment Table 4 is a long air breathing table requiring 38 hours, 11 minutes to complete, and as mentioned above, is sometimes started in the event additional treatment is required at 165 fsw (50 msw) during a Table 6a. Rather than following this table throughout, when it is used, it is common practice to decompress to 60 fsw according to the table and then to switch to a Table 6 at 60 fsw (50 msw). Decompression can then proceed via Table 6 with all appropriate oxygen breathing extensions to the surface. In certain specially equipped facilities, enriched air ("nitrox") and heliox mixtures, designed to maintain a PO2 of 2.8 ATA (40% oxygen) are used at 165 fsw (18 msw) to reduce the amount of additional inert gas loading during treatment.

Treatment table 7 is shown in the Figure 5 below. This table is used only as a last resort, when the severity of the symptoms are such that residual impairment or loss of life may result if the currently prescribed decompression from 60 fsw is undertaken. Examples include complete paralysis of limbs, coma, and/or loss of spontaneous respirations. It should not be used for residual symptoms such as changes in sensation termed paresthesia, limb weakness where the patient can move the limb against gravity, or when loss of bladder control occurs without limb paralysis. These symptoms often respond to repeated daily hyperbaric oxygen treatments according to treatment Tables 5 or 6.

As can be seen from the figure, treatment length is at least 48 hours. Such lengthy treatment requires a special facility and adequate personnel to support such treatment. In general the treatment chamber should be a multiplace chamber with both inner and outer locks to allow personnel to enter or leave the chamber and supplies to be locked down to the divers. Because of the extensive and slow decompression required, a life support system or air supply system and an appropriate back-up are needed to support this table. Loss of air supply and the need to return to the surface will result in recurrence of bends, usually with worsening of symptoms and the development of bends in the patient’s attendants.

Oxygen Toxicity

Oxygen toxicity may develop during treatment, particularly when the oxygen treatment tables are used. Toxicity may take two forms: 1) central nervous system toxicity and 2) pulmonary toxicity. Warning signs of CNS oxygen toxicity include tunnel vision; abnormal ringing or roaring sounds in the ears; nausea; muscle twitching, usually in the lips or face; dizziness; and change in behavior, including confusion, though these cannot be relied on; CNS toxicity frequently ocurrs without warning. If oxygen breathing is continued, a generalized seizure will occur. For the resting chamber patient, CNS oxygen toxicity is unlikely at depths of 50 fsw (15 msw while breathing pure. PO2 =2.5 atm) or shallower, and extremely unlikely at depths of 30 fsw (9 msw) and shallower. If signs of CNS toxicity develop, oxygen breathing is stopped, and the patient is allowed to breath chamber air. Oxygen administration can be restarted 15 minutes after all symptoms have resided.

Pulmonary oxygen toxicity is manifested by symptoms of chest discomfort and burning, particularly on deep inhalation. It is the result of lung irritation as a result of breathing oxygen with a partial pressure above 0.5 atm.&endash;equivalent to breathing 50% oxygen on the surface for prolonged periods of time. Generally, the administration of a single treatment Table 6 does not cause pulmonary oxygen toxicity unless a significant amount of oxygen was breathed during the previous dive or during transport for treatment. It is rarely a major risk factor, nor does it usually require action when it does ocurr.

Recurrences

Recurrences of symptoms or worsening of incompletely resolved symptoms may occur during the decompression phases of treatment, or shortly after treatment is completed. This happens most frequently after treatment Table 5. For recurrences during treatment, the patients should be recompressed to the depth from which decompression had begun, usually 60 fsw for Tables 5 or 6. The table is then either repeated at that depth, or an alternate more conservative treatment schedule is selected (i.e., treatment Table 6 instead of Table 5, or treatment Table 6 with extensions).

Adjunctive therapy

Many bend patients are dehydrated from water loss due to immersion or from tissue swelling caused by the disease process. Most bends patients will benefit from hydration. Conscious individuals may take fluids by mouth, but those who are severely ill or unconscious will require intravenous therapy.

Steroids have been used often in an attempt to reduce CNS edema in severe cases of spinal cord DCI, but they do not seem to be helpful. Similarly the use of other drugs, such as aspirin, to reduce platelet adhesiveness and the tendency of blood to clot have been proposed, but none of these have been conclusively shown to be helpful. In fact most research has indicated that for most of these therapies to be useful in preventing the secondary effects of an illness, they usually must be given prior to the initiating event.

Residual symptoms

When the time from the onset of symptoms until recompression is begun is long, DCI symptoms often will not resolve completely during initial treatment. Residual symptoms may be treated by once-daily administration of treatment Table 6 or twice-daily therapy on treatment Table 5 as long as improvement is achieved. Some further resolution of symptoms may continue once treatment is terminated. However, in severe cases&endash;especially of spinal cord involvement&endash;complete recovery cannot be assured.

Flying after treatment

Current U.S. Navy recommendations are that divers not fly for 24 hours after treatment for pain-only DCI where all symptoms were resolved; for 48 hours for neurological DCI with complete relief; and for 72 hours when Table 4 was used, or when the diver has residual symptoms from treatment.

When evacuating a patient to a treatment facility, or immediately after completing initial treatment, the individual should be flown in a plane that can be pressurized to 1 atm or as low as possible in an unpressurized aircraft.

Conclusion

This article describes U.S. Navy practices in the treatment of decompression illness. Although tables used by other navies and diving organizations may vary, many are similar to those described above. Also, the educated diver will realize that much of the data, upon which these procedures are based, is empirical; many of the recommendations e.g. flying after treatment, come from physicians rather than from a carefully conducted research study. As a result, the recommendations contained here may change as new information is obtained. The experienced diving physician should apply them as most appropriate for the individual case; the exact treatment given an individual diver may vary, and of course, if in doubt, should seek out appropriate expert help.

Dr. John Zumrick is an active cave diver and practicing anethesiologist with the U.S. Navy. Prior to serving his residency at Bethesda Naval Hospital, he served as a medical officer at the Navy's Experimental Diving Unit in Panama City, Florida. He can be contacted at: 1588 Chain Ferry Way, Orange park, FL 32073.

References:

US Navy Manual