Guiding Principles in Choosing a Therapeutic Table for DCI Hyperbaric Therapy
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MINERVA MEDICA COPYRIGHT® MINERVA ANESTESIOL 2009;75:151-61 REVIEW ARTICLE Guiding principles in choosing a therapeutic table for DCI hyperbaric therapy C. ANTONELLI 1, F. FRANCHI 2, M. E. DELLA MARTA 3, A. CARINCI 4, G. SBRANA 2, P. TANASI 1, L. DE FINA 1, M. BRAUZZI 1 1Unit of Diving and Hyperbaric Medicine, Misericordia Hospital, Grosseto, Italy; 2Postgraduate School of Anesthesiology and Intensive Care, University of Siena, Siena, Italy; 3Unit of Orthopedics and Traumatology, Hospital of Stradella, Pavia General Hospital, Pavia, Italy; 4Unit of Acceptance and Urgency Medicine and Surgery, Hospital of Atessa, Lanciano-Vasto General Hospital, Lanciano, Chieti, Italy ABSTRACT Hyperbaric therapy is the basis of treatment for pervasive development disorders. For this reason, the choice of the right therapeutic table for each case is critical. Above all, the delay in recompression time with respect to the first symp- toms and to the severity of the case must be considered. In our experience, the use of low-pressure oxygen tables resolves almost all cases if recompression takes place within a short time. When recompression is possible almost imme- diately, the mechanical effect of reduction on bubble volume due to pressure is of remarkable importance. In these cas- es, high-pressure tables can be considered. These tables can also be used in severe spinal-cord decompression sickness. The preferred breathing mixture is still disputed. Heliox seems to be favored because it causes fewer problems during the recompression of divers, and above all, because nitrox can cause narcosis and contributes nitrogen. Saturation treatment should be avoided or at least used only in special cases. In cases of arterial gas embolism cerebral injury, it is recommended to start with an initial 6 ATA recompression only if the time between symptom onset and the begin- ning of recompression is less than a few hours. Key words: Hyperbaric oxygenation - Decompression - Tables. n the therapeutic treatment of decompression 100% oxygen can be breathed with a low proba- Iillness (DCI), hyperbaric therapy has a promi- bility of oxygen toxicity. Thus, both treated divers nent role; therefore, the choice of the correct ther- and the staff who attend to them in the chamber apeutic table for each case is very important. can be quickly decompressed. The most widely Several recompression schedules (commonly used of these tables are USN5 and USN6 or a sim- referred to as “treatment tables”) have been empir- ilar equivalent. These tables have algorithms that ically developed, based on statistics or tests in allow breathing oxygen at 2.8 ATA and at 1.9 ATA. healthy individuals (e.g., Van Der Aue Tables of The USN6 table can be extended to provide addi- 1945). The initial experience of recompression tional breathing cycles at both depths. An extreme with oxygen tables equivalent to 18 m deep had so example of this is the Catalina table, in which up much success that it became the basis of modern to eight cycles of oxygen can be administered at recompression therapy.1 At 2.8 ATA pressure, 18 m, and 18 cycles can be administered at 9 m. Vol. 75 - No. 3 MINERVA ANESTESIOLOGICA 151 MINERVA MEDICA COPYRIGHT® ANTONELLI THERAPEUTIC TABLE FOR DCI HYPERBARIC THERAPY Many cases of DCI taking place on the surface used in stabilized neurological conditions or resid- can be compressed with satisfactory results using ual painful symptoms.6, 7 In this treatment, the the equivalent 18 m deep pressure while the patient chamber remains under pressure until clinical sta- breathes 100% oxygen, using one of the princi- bilization is reached, usually 12 h or longer. When pal treatment schemes available. U.S. Navy guide- the saturation treatment begins, decompression lines advise the use of table 5 only for mild DCI, must be performed only when a large improve- and symptoms must resolve within 10 min after ment is achieved. Other saturation depths have reaching 18 m. For all other situations, a differ- been proposed and may be compulsory for indi- ent table must be used, usually USN6. viduals decompressing from either deep bounce Most practitioners prefer to use the USN6 table dives or saturation dives.8 In such situations, the for all instances of DCI. Most DCI cases in divers environmental pressure and the treatment gases originating at the surface, therefore, can be man- pressure must be mixed so that the partial pressure aged using USN5 tables, USN6 tables or USN6 of oxygen does not rise above the limits of 0.5 tables with extensions.2 Oxygen cycles are admin- ATA (usually 0.35-4 ATA) and 2.8 ATA, respec- istered at 18 m until the symptoms are relieved or tively. until the patient is clinically stable, for a maxi- Immediate recompression has the greatest suc- mum time allowed by guidelines of the particu- cess, and delays in treatment tend to worsen the lar table. A single treatment is often sufficient to prognosis.9 The effect of delays on the long-term resolve symptoms completely; however, in the case outcome in individual cases, however, is unpre- of residual clinical signs and symptoms, supple- dictable. Although there is partial agreement in mentary treatments must be administered. An the international scientific community about the analysis report by the Divers Alert Network (DAN) effect of delays, it is still a matter of debate. The suggested that this result was probably achieved points of contention are the pressure and the with no more than seven treatments.3 In divers with breathing gas. Pressure reduces bubble volume by severe neurological DCI, however, a greater num- a simple mechanical effect. According to ber of treatments may be required to reach maxi- Bergmann, the maximum bubble reduction is for mum results on the treatment plateau. Multiple pressure from 4 to 6 ATA. Beyond this depth, there recompressions for isolated musculoskeletal (pain is no further benefit. only) DCI are usually not recommended. Generally, the therapeutic pressures used do not More severe cases can be managed using a deep- allow the disappearance of intravascular gaseous er option, e.g., the Comex table 30 or 50, in which sleeves formed by bubble confluence, but they pressurization is 30 or 50 m depth, respectively, cause fragmentation and re-direct the gaseous and breathed oxygen is mixed with helium or embolus into the circulation, releasing collateral nitrogen. Animal studies 4 and a published case vessels. Recompression acts on the primary dis- review 5 provide little evidence in favor of treat- ease cause, but not on its secondary effects. ment at pressures >2.8 ATA. After bubbles have Furthermore, the recompression determines new induced secondary pathophysiologic changes, inert gas tissue saturation and requires appropri- reduction in bubble size is just one part of a com- ate decompression.10 In the past, the optimal depth plex therapy, which might include hyperoxygena- was considered 3 ATA. On a USN initiative and tion, rehydration and pharmacotherapy. as a consequence of animal testing conducted by If the chamber complex and staff are capable of Leitch et al., however, it was reduced to 18 m.11 supporting saturation therapy, it should only be The 18-m treatment may be considered too used when the severity of the symptoms are such deep or too shallow. The initial studies of Behnke that marked residual impairment or loss of life et al. seemed to indicate that 10 m was adequate may result if decompression from 60 feet is under- for all cases.12 On the other hand, the human tri- taken.6 These should not be used in the presence als conducted by Goodman et al. indicated that a of numbness, tingling, decreased sensation of shallow treatment depth was associated with a high touch, hypesthesia, limb weakness or bladder treatment failure rate.13 Wilson et al. reported 65 problems without limb paralysis. It is not to be DCI cases treated on 100% oxygen at either 18 152 MINERVA ANESTESIOLOGICA March 2009 MINERVA MEDICA COPYRIGHT® THERAPEUTIC TABLE FOR DCI HYPERBARIC THERAPY ANTONELLI m or 14 m for three 30-min O2 breathing peri- ods. Only 16% of the patients treated at 18 m had Bubbles recurrent symptoms, while 40% of the patient treated with the 14 m table had recurrences.14 Depths >18 m appear to be beneficial, provided Hypoxia there are no hardware restrictions. Anecdotal evi- dence and isolated case reports describe the ben- efits of increased pressure, but there are no report- Endothelial stress ed trials large enough to draw firm conclusions.15 Some authors have also had experiences where Nitric oxide superoxide anion there was rapid resolution of symptoms soon after compression to 50 m, which showed little or no resolution after several hours at 18 m. According Peroxynitrite to several authors, many cases of DCI resolve dur- ing compression to 18 m, especially if treated rap- idly. The available evidence suggests that treat- Perivascular oxidative stress ment at depths shallower than 18 m runs the risk of treatment failure and that treatments deeper than 18 m offer no particular benefit in the major- Activation of leucocytes and endothelial adhesion ity of cases.16 For spinal cord DCI treatment, we must consid- er that hyperbaric oxygen is thought to be able to Figure 1.—Mechanism of activation of leucocytes and endothe- improve reperfusion injury (symptom deterioration lial adhesion. during compression), while it also has beneficial effects in cases of tissue ischemia or inflammato- because it is metabolized by tissues and, therefore, ry phenomena. The effect of the therapy, there- does not accumulate like an inert gas does. This fore, results from an optimal relationship between results in a reduction of the total gas pressure in the the positive and negative effects of the hyperbar- tissues surrounding the bubble, enhancing the rate ic oxygen.