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Taravana: Fact or Falacy?

A unique form of decompression illness associated with breath-hold diving is discussed, including research and recommendations.
Decompression illness (DCI) is mainly associated with compressed gas diving or caisson work. However, since 1965, diving researchers have become increasingly aware of a curious cluster of neurological symptoms associated with breath-hold diving, but not attributed to hypoxia of ascent [1,2]. The condition, known as “taravana” amongst pearl divers of the Tuamotus (a chain of islands and atolls in French Polynesia), has increasingly become accepted as a unique form of DCI [3]. The typical presentation is a rapid onset of partial paralysis, visual problems, difficulties with hearing or speech [3], and even cases of loss of consciousness and death [4]. Although scans have confirmed that it is an injury to the brain [5,8], the underlying mechanism is not completely understood. For instance, it is not clear whether it is primarily the result of arterial gas embolism [9,10], or due to the formation of inert gas bubbles within the brain itself [4,11]. Either one or both of these mechanisms may be involved in developing taravana; conceivably, it might also be something much more complicated than the usual dichotomous understanding [12].
Bubble detection methods have been used quite widely to assess decompression stress. Similarly, they have been employed to predict the chances of developing decompression disorders following decompression. Of the various available methods, precordial Doppler and cardiac ultrasound are the best known. Doppler detections have confirmed the presence of bubbles in breath-hold divers [11]. However, Doppler bubblefindings have been somewhat at odds with the severity of symptoms that have been reported. Also, recent advances in ultrasound technology have made it more feasible to use cardiac ultrasound to better quantify the risk.
In 2013, the author of this article, together with a team of DAN Europe researchers, was able to show significant intracardiac bubbles following breath-hold diving using a two-dimensional cardiac ultrasound. Using conventional cardiac ultrasound methods and an established scoring method [13], significant bubbles were observed in a group of spearfishermen after performing repetitive breath-hold dives under laboratory conditions. Based on this discovery, the team decided to employ a well-recognised decompression algorithm to determine if it would be able to predict the accumulation of inert gas during breath-hold diving excursions associated with detectable bubbles. If so, and ifpost-diving bubbles could be predicted mathematically, this might suggest that the risks for developing taravana might be minimised by following the same principles used for safe decompression after compressed gas diving.
With this objective in mind, various repetitive breath-hold dive profiles were recorded for depth, dive time, bottom time, descent and ascent rates and gradient factors1 (GF), all calculated through the use of the Bühlmann ZH-16 Model C[13,14]. However, most of the profiles had very low GF,typically 33% or less of the maximum value. This approach seems unable to predict the appearance of inert gas bubblesfollowing breath-hold diving. Therefore, there is reason to suspect additional predisposing mechanisms. Something else must be involved that makes breath-hold divers uniquely vulnerable compared to the inert gas dynamics associated with compressed gas diving.
In evaluating various spearfishing divers, the physiology of breath-hold diving, and the specific practices associated with taravana, a new theory has emerged. It would seem that it may be due to the following factors, namely the pooling of blood in the lungs during the dive with an associated additional uptake of inert gas from the lungs to the blood. This would be followed by a rapid shift of blood upon returning to the surface that might explain the level of bubbles observed in the heart even in the absence of significantly elevated tissue inert gas saturations as would be predicted by usual decompression algorithms.
Based on this research, the following recommendations have been made:
  • Breath-hold diving has become increasingly popular in recent years. Those involved in the sport push towards ever-increasing depths (particularly those who engage in either competitive breath-hold diving or spearfishing). As a result, the incidence of taravana is expected to increase, unless additional precautionary measures are introduced as normative practice.
  • Even though the risk for developing taravana cannot be predicted using traditional decompression modelling, this does not mean that recommendations cannot be made. In as far back as 1965 a “surface recovery time” of at least three times the total breath-hold dive time wasrecommended by the United States Navy [15]. Therefore, in lieu of more specific advice, it is also recommended thatalthough the exact cause may be elusive to some extent,the manifestations of taravana are consistent with DCI. The same first aid and treatment measures are therefore recommended: 100% oxygen first aid and prompt referral for recompression for neurological symptoms following deep, repetitive breath-hold diving.
The main conclusions of this research are threefold:
  • Significant intracardiac bubbling has been observed following repetitive breath-hold diving. This supports the idea of a bubble-related cause of taravana.
  • Current decompression models are unsuitable for predicting breath-hold related bubbles and, consequently, the risk of developing taravana.
  • It is noteworthy that the experimental dive profiles used for the study, which produced bubbling, are moreconservative than those used regularly in the open ocean. Until we find better predictors of taravana, we strongly recommend that all divers follow the empirical precautionary principle of spending at least three times the duration of their dive at the surface in order to recover.
Research is ongoing. Breath-hold divers who are interested in participating in this research are welcome to
  • Gradient factors (GF) are an expression of inert gas supersaturation of theoretical tissues or compartments within the body during ascent and surfacing. They offer a mathematically manageable method of determining which of these theoretical compartments appear most vulnerable to bubble formation, for example, the leading tissues or compartments. During the original table development, and based on actual testing, maximum GFs were determined for each of the theoretical tissues which have been expressed as maximum values (or M-values) of inert gas saturation for the 16 “tissues” considered by the Bühlmann ZH-16 Model C.
  • Cross, E.R. 1965. Physiology of Breath-Hold Diving and the Ama of Japan. In: Rahn H, Yokoyama T. (eds.). Taravana diving syndrome in the Tuamotu diver. Washington, DC: National Academy of Sciences Research Council.
  • Paulev, P. 1965. Decompression sickness following repeated breath-hold dives. J Appl Physiol (1985), 20(5): 1028-31.
  • Lemaitre, F., Fahlman, A., Gardette, B. & Kohshi, K. 2009. Decompression sickness in breath-hold divers: a review. J Sports Sci, 27(14):1519-1534.
  • Moon, R.E. & Gray, L.L. 2010. Breath-hold diving and cerebral decompression illness. Undersea Hyperb Med, 37(1):1-5.
  • Kohshi, K., Katoh, T., Abe, H. & Okudera, T. 2000. Neurological accidents caused by repetitive breath-hold dives: two case reports. J Neurol Sci, 178(1):66-69.
  • Kohshi, K., Kinoshita, Y., Abe, H. & Okudera, T. 1998. Multiple cerebral infarction in Japanese breath-hold divers: two case reports. Mt Sinai J Med, 65(4):280-283.
  • Kohshi, K., Wong, R.M., Abe, H., Katoh, T., Okudera, T. & Mano, Y. 2005. Neurological manifestations in Japanese Ama divers. Undersea Hyperb Med, 32(1):11-20.
  • Kohshi, K., Wong, R.M., Higashi, T., Katoh, T. & Mano, Y. 2005. Acute decompression illness following hyperbaric exposure: clinical features of central nervous system involvement. J UOEH, 27(3): 249-261.
  • Lindholm, P. & Lundgren, C.E. 2009. The physiology and pathophysiology of human breath-hold diving. J Appl Physiol (1985), 106(1):284-292.
  • Liner, M.H. & Andersson, J.P. 2010. Suspected arterial gas embolism after glossopharyngeal insufflation in a breath-hold diver. Aviat Space Environ Med, 81(1):74-76.
  • Prediletto, R., Fornai, E., Catapano, G., Carli, C., Garbella, E., Passera, M., Cialoni, D., Bedini, R. & L’Abbate, A. 2009. Time course of carbon monoxide transfer factor after breath-hold diving. Undersea Hyperb Med, 36(2):93-101.
  • Thom, S.R., Bennett, M, & Banham, N.D., Chin, W., Blake, D.F., Rosen, A., Pollock, N.W., Madden, D., Barak, O., Marroni, A., Balestra, C., Germonpré,P., Pieri, M., Cialoni, D., Le, P.J., Logue, C., Lambert, D., Hardy, K.R., Sward, D., Yang, M. Bhopale, V.B. & Dujic, Z. 2015. Association of microparticles and neutrophil activation with decompression sickness. J Appl Physiol (1985), 119(5):427-434.
  • Blogg, S.L., Gennser, M., Mollerlokken, A. & Brubakk, A.O. Ultrasound detection of vascular decompression bubbles: the influence of newtechnology and considerations on bubble load. Diving Hyperb Med 2014, 44(1):35-44.
  • Germonpré, P., Papadopoulou, V., Hemelryck, W., Obied, G., Lafère, P., Eckersley, R.J. Tang, M.X. & Balestra, C. 2014. The use of portable 2D echocardiography and ‘frame-based’ bubble counting as a tool to evaluate diving decompression stress. Diving Hyperb Med, 44(1):5-13.
  • Lanphier, E.H. 1965. Application of decompression tables to repeated breath-hold dives. Washington, DC: National Academy of Sciences, National Research Council.


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