The Undersea and Hyperbaric Medical Society (UHMS) is an international non-profit organization serving members from more than 50 countries. The UHMS is the primary source of scientific information for diving and hyperbaric medicine physiology worldwide.

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Featured News

Saturday, June 30




8:00 AM - 10:00 AM

Enrico Camporesi, MD
"Hyperbaric Oxygen Therapy for Aseptic Necrosis of the Femoral Head andof the Femoral Condyli"

camporesi image     Osteonecrosis of the knee (ONK) is a form of aseptic necrosis resulting from ischemia to subchondral bone tissue. Typically, common surgical treatments are invasive and palliative or time-limited. Hyperbaric oxygen (HBO2) therapy may provide a non-invasive alternative by improving oxygenation and reperfusion of ischemic areas, both for distal femoral condyli, as recently described, or for a similar malady of the femoral head, previously published.
     We recently described 37 ONK patients (29 male, 8 female; mean age ±1 SD: 54±14). 83.7% of patients presented with Aglietti stage I-II; 16.3% presented with Aglietti Stage III.  Patients were treated with HBO2 once a day, five days a week, at 2.5 ATA with 100% inspired oxygen by mask for an average of 67.9±15 sessions. Magnetic resonance imaging was performed before HBO2, within one year after completion of HBO2, and in 14 patients, 7 years after treatment. Oxford Knee Scores (OKS), an index of functionality, where 60 is normal,  were recorded before HBO2 and at the end of each HBO2 treatment cycle.
     After the 30 sessions of HBO2, 86% of patients experienced improvement in their OKS, 11% worsened, and 3% did not change. All patients improved in OKS after 50 sessions. MRI evaluation 1 year after HBO2 completion showed that edema at the femoral condyle had resolved in all but one patient. MRI at 7 year after completing therapy were all normal. In conclusion, HBO2 is beneficial in ONK. Patients experienced improvements in pain and mobility as demonstrated by improvement in OKS. Radiographic improvements were also seen upon post treatment follow-up. Aglietti staging for the entire sample saw an aggregate decrease (p < 0.01) from 1.7 ± 0.7 to 0.3 ± 0.6.

Gerardo Bosco, MD
"Hyperbaric pre-conditioning"
Bosco image
Pre-conditioning (PC) has been described as the hyperbaric oxygen (HBO2) experience before a critical event, with the aim to prevent a specific clinical condition, and its development as a valuable complement both in diving medicine (Bosco, 2010) as well as prior to ischemic or inflammatory situations. PC is a preventive treatment that triggers endogenous cascades, which can protect from stress-activated and stress-reactive responses. A possible mechanism of HBO-PC mediating beneficial effects has been described as attenuation of the production of proinflammatory cytokines in response to an inflammatory stimulus such as surgery and modulation of the immune response. HBO-PC protocols are performed at 2.0–2.5 atmospheres absolute (ATA), and usually only applied for one or a few days. The physical adaptations in response to alterations in atmospheric oxygen appear to extend not only to survival, but also a preconditioned state.
     Similar to ischemic and stress preconditioning, many different paradigms have been used to demonstrate that either rapid or delayed tolerance is affected by the HBO2 therapy. Irrespective of the cause of injury, inflammatory cytokines released after the primary event trigger leukocyte activation and free radical release, causing secondary damage and extension of injury. Thus, modulating inflammatory molecules has the potential benefit of limiting leukocyte-mediated extension of injury. Many studies demonstrated a protective mechanism of HBO-PC in the injured brain, heart, or liver. Previous data by Yang and colleagues on animals demonstrated that HBO2 inhibits TNF-α production during intestinal, brain and muscle ischemia-reperfusion and it has a beneficial effect, mediated by decreased production of IL-6, IL-1β, dopamine and lactate (Bosco, 2007; Yang, 2001;2006;2010). Studies on animals showed that HBO-PC can protect the brain from ischemia-reperfusion injury and that Sirt1 is a potential molecular target for therapeutic approaches (Ding, 2017). In man, HBO-PC induces endogenous cardioprotection subsequent to ischemic reperfusion injury (Allen, 2014).
     Additionally, clinical HBO-PC showed effects before surgery. A single preoperative hyperbaric oxygen treatment on the day before surgery may reduce the complication rate in pancreatic resection (Bosco, 2014). In liver surgery, studies demonstrated to increase the number of new cells and the density of microcirculation in the regenerating liver after HBO-PC (Theodoraki, 2011). Furthermore, hyperbaric oxygen preconditioning improves postoperative dysfunctions by reducing oxidant stress and inflammation (Gao, 2017). A recent experimental paper has identified an important mechanism involved in triggering the beneficial effect of HBO-PC, as the intracellular induction of heme-oxygenase-1 in hepatic IR injury. Moreover, in dive medicine HBO-PC reduced bubble formation and platelets activation; HBO-PC might enhance lymphocyte antioxidant activity and reduce reactive oxygen species levels. Pre-breathing oxygen in water may also preserve calcium homeostasis, suggesting a protective role in the physiological lymphocyte cell functions (Bosco, 2010; Morabito, 2011).

     Whether the various preconditioning protocols contribute to the different results should be investigated in further studies and applied to diverse surgical procedures, especially major surgeries leading to postoperative ICU admission. Therefore, HBO-PC is an encouraging and feasible therapeutic strategy for protecting organs from the subsequent lethal stimulus.
  1. Ding P, Ren D, He S, He M, et al (2017). Sirt1 mediates improvement in cognitive defects induced by focal cerebral ischemia following hyperbaric oxygen preconditioning in rats. Physiological research, 66(6).
  2. Yang ZJ, Bosco G, Montante A, Ou XL and Camporesi EM (2001) Hyperbaric O2 reduces intestinal ischemia-reperfusion-induced TNF-a production and lung neutrophil sequestration. Eur J Appl Physiol 85: 96-103
  3. Yang Z, Nandi J, Wang G, Bosco G, et al. (2006) Hyperbaric Oxygenation ameliorates indomethacin-induced enteropaty in rats by modulating TNF-a and IL-1 b production. Dig Dis Sci 34(1-2):70-6.
  4. Bosco G, Zj Yang, J Nandi, Jp Wang, et al. (2007) Effects of hyperbaric oxygen on glucose, lactate, glycerol and antioxidant enzymes in the skeletal muscle of rats during ischemia and reperfusion. Clin Exp Pharmacol Physiol 34, 70-76.
  5. Yang Zj, Bosco G, Xie Y, Chen Y, Camporesi EM. (2010) Hyperbaric oxygenation alleviates MCAO-induced brain injury and reduces hydroxyl radical formation and glutamate release. Eur J Appl Physiol. Feb;108(3):513-22.
  6. Bosco G, Yang Zj, Di Tano G, Camporesi EM, et al. (2010) Effect of in-water versus normobaric oxygen pre-breathing on decompression-induced bubble formation and platelet activation. J Appl Physiol. May;108(5):1077-83.
  7. Morabito C, Bosco G, Pilla R, Corona C, et al. (2011) Effect of pre-breathing oxygen at different depth on oxydative status and calcium concentration in lymphocytes of scuba divers. Acta Physiol (Oxf). May;202(1):69-78.
  1. Bosco G, Casarotto A, Nasole E, Camporesi E, et al. (2014). Preconditioning with hyperbaric oxygen in pancreaticoduodenectomy: a randomized double-blind pilot study. Anticancer research, 34(6), 2899-2906.
  2. Theodoraki K, Tympa A, Karmaniolou I, Tsaroucha A, et al. (2011). Ischemia/reperfusion injury in liver resection: a review of preconditioning methods. Surgery Today, 41(5), 620.
  3. Gao Z. X, Rao J, & Li Y. H. (2017). Hyperbaric oxygen preconditioning improves postoperative cognitive dysfunction by reducing oxidant stress and inflammation. Neural regeneration research, 12(2), 329.
  4. Allen M, Golembe E, Gorenstein S, Butler G. Protective effects of hyperbaric oxygen therapy (HBO2) in cardiac care-A proposal to conduct a study into the effects of hyperbaric pre-conditioning in elective coronary artery bypass graft surgery (CABG) Undersea Hyperb Med. 2014;42:107–114.

Shai Efrati, MD
"Brain injury"


  1. Basics pathophysiological cascade of non-recoverable brain injuries.
  2. The neuroplasticity effect of hyperbaric oxygen therapy
  3. Selecting the optimal candidate for the treatment

Clinical studies published in recent years present convincing evidences that hyperbaric oxygen (HBO2) therapy can be the coveted neurotherapeutic method for brain repair of neurological incidents like traumatic brain injury and stroke. This new understanding leads to a paradigm change in the way that we refer to chronic brain injuries; from now these should be thought of like other non-healing wounds in other parts of the body.
     The classical candidate for HBO2 is a patient with unrecovered brain injury where tissue hypoxia is the limiting factor for the regeneration process. In this patient, HBO2 may induce neuroplasticity in the stunned regions where there is a brain anatomy/physiology mismatch (as for example PET/MRI).
     In this lecture we will discuss the multifaceted role HBO2 can play in neurotherapeutics based on recent persuasive evidence demonstrating HBO2 efficacy in brain repair as well as a new understanding of brain energy management and response to brain damage. We will also discuss how to select suitable candidates and how to choose the optimal HBO2 protocol for the selected candidate.

Panel Discussion

1:00 PM - 2:00 PM

Brian Keuski, MD; Fellow, Duke Hyperbarics
"Diving medicine literature update"

headshot Keuski

Take a whirlwind tour through the last 12 months of diving medicine literature. Major topics include: decompression illness, fitness to dive issues, immersion pulmonary edema, and diving physiology.

Lince Varughese, MD; Fellow, LSU Hyperbarics
"Hyperbaric medicine literature update"

Lince Varughese MD

Dr. Varughese will give a brief update on key articles in recent hyperbaric medicine literature; novel ideas and newfound wisdom.

4:00 PM - 5:00 PM

Gerardo Bosco, MD
"Adaptive mechanisms in breath-hold divers"

Bosco imageThe human body faces extreme physiological challenges while immersed with voluntary breath-holding. Breath-hold diving is potentially associated to extreme environmental factors such as increased hydrostatic pressure, hypoxia, hypercapnia, hypothermia and strenuous exercise. Physiological adaptations can depend among the time of breath suspension and the depth of diving. While descending chest squeeze and blood redistribution occur. Indeed, blood as being an incompressible fluid from peripheral circulation is shifted to the chest. The intrathoracic blood volume increases. Moreover, face immersion results in induced bradycardia, due to the diving reflex. Conversely, breath-holding at rest, out of water, induces non-significant changes in heart rate. Breath-hold swimming, even on the surface, instead causes pronounced bradycardia. During deep diving a higher O2 consumption and a fall in alveolar and blood O2 content was observed. Consequently, alveolar CO2 pressure increases due to chest compression while descending.
     It was supposed that the maximum reachable depth in breath-hold diving was determined by the relationship between total lung capacity and residual volume. Craig suggested a compensatory physiologic mechanism to explain why thoracic implosion does not occur and hypothesized that a certain amount of blood was diverted from the peripheral circulation into the chest. Intrathoracic pressure in such a condition represented the elastic behavior of the chest wall when exposed to high hydrostatic pressure. The increased hydrostatic pressure at depth reduces pulmonary gas volumes and consequently increases intrathoracic blood volume, with enlargement of the right heart chambers and pressures. On the contrary, the left sections of the heart do not undergo any enlargement, and do not show any sign of pressure increase. The systolic stroke volume is the consequence of Starling’s law: the blood shift stretches the heart and increases the intracardiac volume. This certainly means that, although rarely exploited in nature, anaerobic metabolic reserve represents a resource for survival of the animal. The same can be said for high-altitude hypoxic environments.
     Another consideration is the “graded response” to breath-hold diving in relation to the level of physiological stress and to the control by the central nervous system. The diving response is a strategic adaptation to hostile environmental conditions common to many animals but human breath-hold divers require knowledge for the safe and health of participants. 

Peter Lindholm, MD
"Pulmonary pathophysiology in deep breath-hold diving"
lindholm image

Deep breath-hold diving may expose the lungs to the limits of known human physiology. We will discuss barotrauma of descent with pulmonary edema, glossopharyngeal hyperinsufflation and arterial gas embolism.

 Alessandro Marroni, MD
"Breaking news on breath-hold diving research"
A.Marroni VHQ small

Recent data from field research on pathophysiology of breath-hold diving will be presented, with a particular focus on breath-hold diving-induced pulmonary edema, Taravana, epidemiology, mechanisms, pathogenetic hypotheses and data on genetic predisposing factors.



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