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Can Breath-hold Diving Cause DCI?

Breath-hold diving (BHD) or freediving is a form of underwater diving that relies on the divers’ ability to hold their breath until resurfacing, rather than on the use of a breathing apparatus such as scuba gear. Freediving, apnea and skin diving are all synonyms for BHD.

BHD has been around for thousands of years. For the past 100 years, however, it has been somewhat eclipsed by technological advancements and the booming industry of scuba diving. Yet, since the turn of the millennium, BHD has started regaining some of the original attraction – perhaps as part of a general shift towards more ‘natural’, environmentally-conscious, contemplative living.

BHD introduces several physiological challenges, including hypoxia, hypercapnia and nitrogen accumulation. Previously Decompression Illness (DCI) was thought to be limited largely to high pressure work or scuba diving. However, and somewhat counter-intuitively, BHD can actually produce DCI. In fact, there is an historic and very well-established relationship between repetitive, deep BHD and neurological problems which are indistinguishable from DCI 1,2. Already in 1965 Dr Ed Lanphier proposed that DCI could affect BHD if deep repetitive dives were done with short surface intervals 3. Yet, and perhaps even because the mechanisms of DCI in scuba diving-related are not fully understood, there remains an aura of ignorance and denial about DCI in BHD’s. 

During a BHD dive, Dalton’s and Henry’s laws still apply: Nitrogen partial pressure in the lungs therefore increases with environmental pressure according to the diver’s depth. Of course, nitrogen makes up only about 80% of the limited volume of gas in the diver’s lungs. Only a minimal actual amount of nitrogen can therefore be absorbed during a single dive, but some inert gas retention does occur. Moreover, as nitrogen elimination from the body at the surface is slower than the rate of absorption at depth, the net result of a series of deep repetitive BHD’s may be a significant accumulation of inert gas. Therefore, if the surface recovery times are too short, the disparity between uptake and elimination will eventually produce critical supersaturation with resulting bubble formation. 

One of the eponyms for BHD-related DCI is ‘Taravana’. The name is attributed to the pearl divers of the Tuamotu Archipelago in Polynesia 2. These divers do 40 to 60 dives in a day to depths of 30 to 42m to gather pearls. Descent times are typically 30 to 50 seconds, with a total dive time of about 100 seconds, and a surface recovery time of 4 to 6 mins. Many of these divers develop a neurological symptom complex nick-named Taravana, which means “to fall crazily” and is used to describe someone who is “crazy because of the sea”. Taravana-like symptoms are not unique to Polynesian BHD divers, however 1. It has been described in the Ama divers of Japan, Mediterranean sport spear-fishermen, and in competitive breath-hold divers worldwide 4. In fact, any form of deep, repetitive BHD may cause Taravana.

The most common symptoms of Taravana are vertigo, vomiting, paresthesia, muscular weakness and paralysis 1,2,4-6. Others include impaired concentration, lethargy, speech disturbances and altered level of consciousness. Symptoms such as visual changes and hearing loss also occur. The Taravana syndrome has caused deaths in some of these divers, and many who have survived have been left with permanent brain and spinal cord injuries 1,2,4-6. Taravana symptoms appear to affect the CNS almost exclusively 4,5. This is unlike DCI related to scuba diving which also involves other organ systems. For instance, musculoskeletal or joint pain associated with ‘the bends’ is not a familiar feature of Taravana. On the other hand, not all the features of Taravana are typical of DCI. This is why other mechanisms -- such as hypoxia (low O2) and hypocapnia (low CO2) -- are emphasized by some experts 6-8. Some Taravana symptoms also only appear early in the diving day; these may reflect initial neurophysiological disturbances due to the rapid cycles of hypoxia and hyperventilation. Later symptoms seem to be more serious and persistent, however: The Ama divers, for instance, experience these symptoms after at least 4 hours diving to depths in excess of 20m, and when the surface interval is shorter than the dive time 1. This suggests that nitrogen accumulation is certainly a contributing factor 4,5. These later presentations of Taravana are also more consistent with a diagnosis of DCI in terms of the response to surface oxygen and recompression 4,5. Other possible mechanisms cannot be dismissed, however, and include cerebral hypoxia, micro-hemorrhages in the brain (due to extreme changes in blood pressure observed in BHD), arterial gas emboli injected into pulmonary capillaries due to lung damage incurred at depth, amongst others 4.

Even though the exact cause – or causes – of Taravana remain elusive, the appearance of intra-cardiac bubbles after BHD has been confirmed experimentally 9-11. This means that there is certainly scientific justification for considering paradoxical venous gas embolization as a cause of Taravana. In another article in this edition of Alert Diver, Dr Danilo Cialoni details his intra-cardiac bubble findings and the safety recommendations of reducing the risks of developing Taravana.

What is certain is that repetitive, deep, BHD may cause permanent brain damage 4,5,8,12

Another consideration is whether BHD after scuba diving is a good idea. Many recreational divers do scuba and BHD on the same day. The central issues are two-fold: That, (1) combining BHD and scuba may cause CO2 retention-related problems and even inadvertent breath-holding while on scuba, especially when BHD and scuba are alternated in quick succession; and (2) that exercise and BHD may interfere with inert gas elimination, which may either extend the period of off-gassing or make it easier for venous gas emboli to be transferred to the arterial system.

Actual evidence oF these concerns is scarce. The risks seem to be small, but BHD is not recommended during the surface interval between successive scuba dives. 

To avoid an increased risk of DCI, BHD’s should limit the number of deep (> 20 m), repetitive dives they do, and keep the surface recovery times to at least three times the total dive time.
Loss of consciousness during ascent is usually due to hypoxia of ascent. However, when neurological symptoms appear at the surface, especially after a series of deep, repetitive BHD’s, DCI (Taravana) should be considered.

DCI is a rare complication in BHD, limited to relatively small number of elite BHD-athletes. Hypoxia of ascent is far more common, and many BHD’s die every year as a result of blacking out near the surface. We therefore want to remind and encourage all BHD’s to follow the standard safety recommendations, including ‘surface buddy’ diving, adequate surface recovery times, limited hyperventilation, and time-based dive times (i.e., not relying on the urge to breathe but on a safe time-limit). 

1. 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.
2. Paulev, P. 1965. Decompression sickness following repeated breath-hold dives. Journal of Applied Physiology, 20(5):1028-1031.
3. Lanphier, E.H. 1965. Application of decompression tables to repeated breath-hold dives. Washington, DC: National Academy of Sciences, National Research Council.
4. Lemaitre, F. Fahlman, A., Gardette, B. & Kohshi, K. 2009. Decompression sickness in breath-hold divers: a review. Journal of Sports Sciences, 27(14):1519-1534.
5. Moon, R.E. & Gray, L.L. 2010. Breath-hold diving and cerebral decompression illness. Undersea and Hyperbaric Medicine, 37(1):1-5.
6. Joulia, F., Lemaitre, F., Fontanari, P., Mille, M.L. & Barthelemy, P. 2009. Circulatory effects of apnoea in elite breath-hold divers. Acta Physiologica (Oxford, England), 197(1):75-82.
7. Cortegiani, A. & Foresta, G. et al. 2013. An atypical case of Taravana syndrome in a breath-hold underwater fishing champion: a case report. Case Reports in Medicine, (5):1-5.
8. Kohshi, K., Katoh, T., Abe, H. & Okudera, T. 2000. Neurological accidents caused by repetitive breath-hold dives: two case reports. Journal of the Neurological Sciences, 178(1):66-69.
9. Blogg, S.L., Gennser, M., Møllerløkken, A. & Brubakk, A.O. 2014. Ultrasound detection of vascular decompression bubbles: the influence of new technology and considerations on bubble load. Diving and Hyperbaric Medicine Journal, 44(1):35-44.
10. Mollerlokken, A., Breskovic, T., Palada, I., Valic, Z., et al. 2011. Observation of increased venous gas emboli after wet dives compared to dry dives. Diving and Hyperbaric Medicine, 41(3):124-128.
11. Alaimo, M., Aiello,G., Marino, E., Zummo, L. & Cappello, F. 2010. Taravana: documentation of bubbles by computerised tomography. Journal of Neurosurgical Anesthesiology, 22(3):271.
12. Kohshi, K., Kinoshita, Y., Abe, H. & Okudera, T. 1998. Multiple cerebral infarction in Japanese breath-hold divers: two case reports. Mount Sinai Journal of Medicine, 65(4):280-283.

1. Bove, F. n.d. Can freediving cause DCS? [Online]. Available at:
ScubaMed/FreedivingCauseDCS.asp [Accessed: 1 August 2017].
2. Cross, E.R. n.d. Taravana in Pearl Divers. [Online]. Available at: [Accessed: 1 August 2017].
3. Denoble, P. n.d. Neurological Injury. [Online]. Available at:[Accessed: 1 August 2017].
4. Denoble, P. 2011. Decompression Sickness Risk: Freediving After Scuba. [Online]. Available at: [Accessed: 1 August 2017].
5. Dubern, R. 2011. Decompression Sickness Risk in Spearfishing vs. Freediving. [Online]. Available at: [Accessed: 1 August 2017].
6. Gempp, E. & Blatteau, J.E. 2006. Neurological Disorders After Repetitive Breath-Hold Diving. [Online]. Available at: [Accessed: 1 August 2017].
7. Kohshi, K. & Wong, R.M. et al. 2005. Neurological manifestations in Japanese Ama divers.
[Online]. Available at: [Accessed: 1 August 2017].
8. Naslund, S. 2009. Apnea and DCS. [Online]. Available at: [Accessed: 1 August 2017].
9. n.d. Decompression Sickness and Breath-hold diving: Is it an issue? [Online]. Previously available at: [Removed].
10. Schipke, J.D., Gams, E. & Kallweit, O. 2006. Decompression sickness following breath-hold diving. [Online]. Available at: [Accessed: 1 August 2017].
11. Stefanidou, S., Melekos, T., Kotsiou, M. & Mesimeris, T. 2013. Decompression sickness related to breath-hold diving: A case report. [Online]. Available at: [Accessed: 1 August 2017].
12. Campbell, E. 1997. Breath-hold Diving: Taravana. [Online]. Available at: [Accessed: 1 August 2017].
13. Editors of Encyclopaedia Britannica. 1998. Taravana syndrome. [Online]. Available at: [Accessed: 1 August 2017].
14. n.a. 2014. Taravana. [Online]. Available at:
[Accessed: 1 August 2017].


Hossam Nasef - October 29th, 2018 at 12:28pm

Thank you for the article, I have some concerns if you don't mind, I would actually consider referring back to the names (DCS) and (AGE) to describe illnesses resulting from BHD, I witnessed and treated a few of these cases that happened after BHD, two of them were in the preparation of a world record in the Red Sea of Egypt, both had one exposure in the day of incident and both were to a depth well more than a hundred meters, both had very serious CNS symptoms and both were diagnosed as AGE that resulted from some lung damage that looked like an over-expansion lung injury which was never suspected in divers who are not breathing compressed gas, I guess that the lungs with all the sophisticated structure will not work as a simple balloon all the time, and partial gas entrapment should have happened in both cases due the rapid ascent, the first case "Benjamin Franz" had massive spinal embolism with paraplegia and the second Patrick Massimo had some kind of multi focal brain infarcts with a list of neurological manifestations!

DAN Medical Team - October 31st, 2018 at 1:27pm

Excellent comments. Your points are well taken. In fact, the author of the article agrees with your concern, and presents the uncertainty in the following paragraph of the original article: "Other possible mechanisms cannot be dismissed, however, and include cerebral hypoxia, micro-hemorrhages in the brain (due to extreme changes in blood pressure observed in BHD), arterial gas emboli injected into pulmonary capillaries due to lung damage incurred at depth, amongst others." The latter mechanism is what you seem to be referring to specifically. Therefore, again in complete agreement with the author, the unique manifestations of BHD-related DCI (i.e, DCS or AGE) require further open-minded research and refinements in terminology. Your comments emphasise this very well.


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