A novel method for tracking nitrogen kinetics in vivo under hyperbaric conditions using radioactive nitrogen-13 gas and positron emission tomography.

Decompression sickness (DCS) is caused by gaseous nitrogen dissolved in tissues forming bubbles during decompression. To date, no method exists to identify nitrogen within tissues, but with advances in positron-emission tomography (PET) technology, it may be possible to track gaseous radionuclides into tissues. We aimed to develop a method to track nitrogen movement in vivo and under hyperbaric pressure that could then be used to further our understanding of DCS using nitrogen-13 (13N2). A single anesthetized female Sprague-Dawley rat was exposed to 625 kPa, composed of air, isoflurane, and 13N2 for 10 min. The PET scanner recorded 13N2 during the hyperbaric exposure with energy windows of 250-750 keV. The PET showed an increase in 13N2 concentration in the lung, heart, and abdominal regions, which all reached a plateau after ∼4 min. This showed that it is possible to gain noninvasive in vivo measurements of nitrogen kinetics through the body while at hyperbaric pressures. Tissue samples showed radioactivity above background levels in the blood, brain, liver, femur, and thigh muscle when assessed using a γ counter. The method can be used to evaluate an array of challenges to our understanding of decompression physiology by quantifying nitrogen load through γ counts of 13N2, and signal intensity of the PET. Further development of the method will improve the specificity of the measured outcomes, and enable it to be used with larger mammals, including humans.NEW & NOTEWORTHY This article describes a method for the in vivo quantification and tracking of nitrogen through the mammalian body whilst exposed to hyperbaric pressure. The method has the potential to further our understanding of decompression sickness, and quantitatively evaluate the effectiveness of both the treatment and prevention of decompression sickness.

Decompression sickness with incidental pulmonary cyst.

Decompression sickness (DCS) is a known complication of scuba diving. DCS occurs when bubbles are formed as pressure is reduced during and after ascent from a dive, following inert gas uptake during the dive. The bubbles cause inflammation and hypoxia. The definitive treatment for decompression sickness is hyperbaric oxygen therapy. We present a case of a healthy 16-year-old male who presented with decompression sickness and an incidental pulmonary cyst discovered by chest CT, likely congenital. The patient was successfully treated with U.S. Navy Treatment Table 6 (TT6) for his decompression sickness, but he continued to have chest pain, requiring hospitalization and consultation with pediatric pulmonology and cardiothoracic surgery from the cyst. Three years later he complained of chest pain with changes in altitude. Chest CT showed persistence of this cyst, and additional cysts. Case conference with pulmonologists and chest radiologist could not offer a definite etiology without lung biopsy, felt to not be indicated. We believe that the changes in pressure/volumes during the dives and TT6 exacerbated his pulmonary cyst.

Persistent extravascular bubbles on radiologic imaging after recompression treatment for decompression sickness: A case report.

Decompression sickness (DCS) is a condition arising when dissolved inert gas in tissue forms extravascular and/or intravascular bubbles during or after depressurisation. Patients are primarily treated with 100% oxygen and recompression, which is often assumed to lead to resolution of bubbles. After this, repeated hyperbaric exposures can be provided in case of persistent symptoms, with oxygen delivery to ischaemic tissues, anti-inflammatory properties and reduction of oedema considered the main mechanisms of action. In this case report we present the history and imaging of a diver diagnosed with DCS that was treated with two US Navy Treatment Table 6 recompressions, but who still had multiple extravascular bubbles apparent on CT-imaging after these hyperbaric treatments. Based on these findings we hypothesise that, contrary to general belief, it is possible that large extravascular bubbles can persist after definitive treatment for DCS.

Decompression illness type II with stroke: challenging situation in acute neurorehabilitation.

A professional 55-year-old female experienced diver, who surfaced after the second dive, had a lucid interval before dropping Glasgow Coma Scale (GCS) to 3/15. She was admitted to intensive care unit and commenced on hyperbaric oxygen therapy. Her initial computed tomography of the head was normal but her magnetic resonance imaging of the brain at 48 hours showed extensive bilateral cortical watershed territory infarcts. She developed acute respiratory distress syndrome which resolved within a few days. Her GCS gradually improved from 3/15 to 6/15, was repatriated to United Kingdom after about 2 weeks of the insult and admitted to a tertiary care hospital where she had myoclonic seizures and was started on anti-epileptics. Then she was transferred to the Rehabilitation Medicine Ward of Leicester General Hospital, with GCS 14/15 with poor sitting balance, for her management and rehabilitation. She had weakness of right upper and lower limbs, dysarthria, neuropathic bilateral shoulder pains, pressure ulcer of left heel, bladder and bowel incontinence and cognitive issues. She improved to have significant neurological recovery within next 3 months, became ambulant independently and bladder and bowel continent. Her Barthel index (from 4 to 17), Montreal Cognitive Assessment Test, Adembrook Cognitive Examination and Berg Balance scale (from 33/56 to 44/56) improved significantly. Early diagnosis, treatment and rehabilitation can have a significant impact on the recovery of decompression illness.

Abdominal decompression illness following repetitive diving: a case report and review of the literature.

The complete pathophysiology of decompression illness is not yet fully understood. What is known is that the longer a diver breathes pressurized air at depth, the more likely nitrogen bubbles are to form once the diver returns to surface [1]. These bubbles have varying mechanical, embolic and biochemical effects on the body. The symptoms produced can be as mild as joint pain or as significant as severe neurologic dysfunction, cardiopulmonary collapse or death. Once clinically diagnosed, decompression illness must be treated rapidly with recompression therapy in a hyperbaric chamber. This case report involves a middle-aged male foreign national who completed three dives, all of which incurred significant bottom time (defined as: "the total elapsed time from the time the diver leaves the surface to the time he/she leaves the bottom)" [2]. The patient began to develop severe abdominal and back pain within 15 minutes of surfacing from his final dive. This case is unique, as his presentation was very concerning for other medical catastrophes that had to be quickly ruled out, prior to establishing the diagnosis of severe decompression illness. After emergency department resuscitation, labs and imaging were obtained; abdominal decompression illness was confirmed by CT, revealing a significant abdominal venous gas burden.

Implementation of Targeted Temperature Management in a Patient with Cerebral Arterial Gas Embolism.

Cerebral arterial gas embolism (CAGE) shows various manifestations according to the quantity of gas and the brain areas affected. The symptoms range from minor motor weakness, headache, and confusion to disorientation, convulsions, hemiparesis, unconsciousness, and coma. A 46-year-old man was transferred to our emergency department due to altered sensorium. Immediately after a controlled ascent from 33 m of seawater, he complained of shortness of breath and rigid extremities, lapsing into unconsciousness. He was intubated at another medical center, where a brain computerized axial tomography scan showed no definitive abnormal findings. Pneumothorax and obstructing lesions were apparent in the left thorax of the computed tomography scan. Following closed thoracostomy, we provided hyperbaric oxygen therapy (HBOT) using U.S. Navy Treatment Table (USN TT) 6A. A brain magnetic resonance imaging diffusion image taken after HBOT showed acute infarction in both middle and posterior cerebral arteries. We implemented targeted temperature management (TTM) to prevent worsening of cerebral function in the intensive care unit. After completing TTM, we repeated HBOT using USN TT5 and started rehabilitation therapy. He fully recovered from the neurological deficits. This is the first case of CAGE treated with TTM and consecutive HBOTs suggesting that TTM might facilitate salvage of the penumbra in severe CAGE.

Observed decompression sickness and venous bubbles following 18-msw dive profiles using RN Table 11.

The venous bubble load in the body after diving may be used to infer risk of decompression sickness (DCS). Retrospective analysis of post-dive bubbling and DCS was made on seven studies. Each of these investigated interventions, using an 18 meters of sea water (msw) air dive profile from Royal Navy Table 11 (Mod Air Table), equivalent to the Norwegian Air tables. A recent neurological DCS case suggested this table was not safe as thought. Two-hundred and twenty (220) man-dives were completed on this profile. Bubble measurements were made following 219 man-dives, using Doppler or 2D ultrasound measurements made on the Kisman-Masurel and Eftedal-Brubakk scales, respectively. The overall median grade was KM/EB 0.5 and the overall median maximum grade was KM/EB 2. Two cases of transient shoulder discomfort ("niggles") were observed (0.9% (95% CL 0.1% - 3.3%)) and were treated with surface oxygen. One dive, for which no bubble measurements were made, resulted in a neurological DCS treated with hyperbaric oxygen. The DCS risk of this profile is below that predicted by models, and comparison of the cumulative incidence of DCS of these data to the large dataset compiled by DCIEM [1, 2] show that the incidence is lower than might be expected.

Elimination of CT-detected gas bubbles derived from decompression illness with abdominal symptoms after a short hyperbaric oxygen treatment in a monoplace chamber: a case report.

We report the case of a 54-year-old male compressed-air worker with gas bubbles detected by computed tomography (CT). He had complained of strong abdominal pain 30 minutes after decompression after working at a pressure equivalent to 17 meters of sea water for three hours. The initial CT images revealed gas bubbles in the intrahepatic portal vein, pulmonary artery and bilateral femoral vein. After the first hyperbaric oxygen treatment (HBO2 at 2.5 atmospheres absolute/ATA for 150 minutes), no bubbles were detected on repeat CT examination. The patient still exhibited abdominal distension, mild hypesthesia and slight muscle weakness in the upper extremities. Two sessions of U.S. Navy Treatment Table 6 (TT6) were performed on Days 6 and 7 after onset. The patient recovered completely on Day 7. This report describes the important role of CT imaging in evaluating intravascular gas bubbles as well as eliminating the diagnosis of other conditions when divers or compressed-air workers experience uncommon symptoms of decompression illness. In addition, a short treatment table of HBO2 using non-TT6 HBO2 treatment may be useful to reduce gas bubbles and the severity of decompression illness in emergent cases.

Decompression illness with hypovolemic shock and neurological failure symptoms after two risky dives: a case report.

Hypovolemia is known to be a predisposing factor of decompression illness (DCI) while diving. The typical clinically impressive neurological symptoms of DCI may distract from other symptoms such as an incipient hypovolemic shock. We report the case of a 61-year-old male Caucasian, who presented with an increasing central and peripheral neural failure syndrome and massive hypovolemia after two risky dives. Computed tomography (CT) scans of the chest and Magnetic resonance imaging scans of the head revealed multiple cerebral and pulmonary thromboembolisms. Transesophageal echocardiography showed a patent foramen ovale (PFO). Furthermore, the patient displayed hypotension as well as prerenal acute kidney injury with elevated levels of creatinine and reduced renal clearance, indicating a hypovolemic shock. Early hyperbaric oxygen (HBO) therapy reduced the neurological deficits. After volume expansion of 11 liters of electrolyte solution (1000 mL/h) the cardiopulmonary and renal function normalized. Hypovolemia increases the risk of DCI during diving and that of hypovolemic shock. Early HBO therapy and fluid replacement is crucial for a favorable outcome.

[Diving Accidents]. / Tauchunfälle.

Decompression injuries occur on account of the special hyperbaric effects during the emerge phase and require superior therapeutic knowledge. Vitally important is emergency treatment with high concentrated oxygen at an early stage. Sever decompression injuries require oxygenation in a hyperbaric treatment chamber.

Echocardiographic evaluation of intracardiac venous gas emboli following in-water recompression.

Decompression sickness is a potentially fatal illness. Optimal treatment is dry recompression with hyperbaric oxygen. In-water recompression (IWR) offers expedited treatment but has insufficient evidence to recommend it as a treatment option. This trial compares IWR to standard surface oxygen treatment using 2D echocardiography as the semi-quantitative measurement for inert gas loading. Divers were randomly assigned to either IWR or normobaric oxygen (NBO2). A provocative dive profile to 33.5 meters for 25 minutes was used to stimulate bubble formation. After 60 minutes on the surface, bubble scoring was obtained using 2D echocardiography. Divers underwent either the IWR or NBO2 treatment for 82 minutes. Echocardiography was then repeated. Pre-treatment mean bubble counts were 28.1 bpf (bubbles per echo frame), [+/- 13.2 to 43.0 95% CI] for IWR, and 18.3 bpf [+/- 0.0 to 39.6 95% CI] for NBO2. After treatment, mean bubble score dropped to 0.1 bpf [+/- 0.0 to 0.2 95% CI] (p < 0.01) and 1.8 bpf [0.0 to 3.8 95% CI] (p = 0.103) respectively. IWR vs. NBO2 reduction of bubble counts was 99.7% vs. 90.1%; however, this was not found to be statistically significant. IWR reduced the central VGE load compared to NBO2, suggesting that IWR is a viable emergency treatment when a recompression chamber is unavailable.

Patent foramen ovale influences the presentation of decompression illness in SCUBA divers.

BACKGROUND: Few have examined the influence of patent foramen ovale (PFO) on the phenotype of decompression illness (DCI) in affected divers. METHODOLOGY: A retrospective review of our database was performed for 75 SCUBA divers over a 10-year period. RESULTS: Overall 4,945 bubble studies were performed at our institution during the study period. Divers with DCI were more likely to have positive bubble studies than other indications (p<0.001). Major DCI was observed significantly more commonly in divers with PFO than those without (18/1,000 v.s. 3/1,000, p=0.02). Divers affected by DCI were also more likely to require a longer course of hyperbaric oxygen therapy (HBOT) if PFO was present (p=0.038). If the patient experienced one or more major DCI symptoms, the odds ratio of PFO being present on a transoesophageal echocardiogram was 3.2 (p=0.02) compared to those who reported no major DCI symptoms. CONCLUSION: PFO is highly prevalent in selected SCUBA divers with DCI, and is associated with a more severe DCI phenotype and longer duration of HBOT. Patients with unexpected DCI with one or more major DCI symptoms should be offered PFO screening if they choose to continue diving, as it may have considerable prognostic and therapeutic implications.

Portal venous gas on computed tomography imaging in patients with decompression sickness.

BACKGROUND: It has been reported that portal venous gas is rarely found on computed tomography (CT) imaging in patients with decompression sickness (DCS). However, we propose that this is not true because we have encountered several patients with DCS who presented with portal venous gas on CT before hyperbaric oxygen therapy (HBOT). Here, we review our charts and present these patients' characteristics. CASES: We treated 37 patients with DCS from April 2007 to September 2011. Nine of these 37 patients underwent CT (thoracic, abdominal, or both) on admission because of dyspnea and other reasons. In four of nine patients, portal venous gas was incidentally found on CT. All patients were male, and three of them were SCUBA (self-contained underwater breathing apparatus) divers. Most of the patients did not have abdominal complaints. Three of four patients presented with gas in other abdominal areas (e.g., mesentery or inferior vena cava). HBOT (United States Navy Treatment Table 6) was performed in all patients, and abdominal CT performed after HBOT in three of four patients revealed the complete disappearance of portal venous gas and other venous gases. One patient died, and the remaining patients survived without any complications. CONCLUSIONS: Most patients with DCS do not require CT examination before HBOT. However, if all patients with DCS undergo abdominal CT, the presence of portal venous gas in these patients may no longer be a rare finding. Although routine CT is not required for patients with DCS, it might be helpful for diagnosis.

Observation of increased venous gas emboli after wet dives compared to dry dives.

INTRODUCTION: Testing of decompression procedures has been performed both in the dry and during immersion, assuming that the results can be directly compared. To test this, the aim of the present paper was to compare the number of venous gas bubbles observed following a short, deep and a shallow, long air dive performed dry in a hyperbaric chamber and following actual dives in open water. METHODS: Fourteen experienced male divers participated in the study; seven performed dry and wet dives to 24 metres' sea water (msw) for 70 minutes; seven divers performed dry and wet dives to 54 msw for 20 minutes. Decompression followed a Bühlmann decompression procedure. Immediately following the dive, pulmonary artery bubble formation was monitored for two hours. The results were graded according to the method of Eftedal and Brubakk. RESULTS: All divers completed the dive protocol, none of them showed any signs of decompression sickness. During the observation period, following the shallow dives, the bubbles increased from 0.1 bubbles per cm ² after the dry dive to 1.4 bubbles per cm ² after the wet dive. Following the deep dives, the bubbles increased from 0.1 bubbles per cm ² in the dry dive to 2.4 bubbles per cm ² in the wet dive. Both results are highly significant (P = 0.0001 or less). CONCLUSIONS: The study has shown that diving in water produces significantly more gas bubble formation than dry diving. The number of venous gas bubbles observed after decompression in water according to a rather conservative procedure, indicates that accepted standard decompression procedures nevertheless induce considerable decompression stress. We suggest that decompression procedures should aim at keeping venous bubble formation as low as possible.

Effect of in-water oxygen prebreathing at different depths on decompression-induced bubble formation and platelet activation.

Effect of in-water oxygen prebreathing at different depths on decompression-induced bubble formation and platelet activation in scuba divers was evaluated. Six volunteers participated in four diving protocols, with 2 wk of recovery between dives. On dive 1, before diving, all divers breathed normally for 20 min at the surface of the sea (Air). On dive 2, before diving, all divers breathed 100% oxygen for 20 min at the surface of the sea [normobaric oxygenation (NBO)]. On dive 3, before diving, all divers breathed 100% O2 for 20 min at 6 m of seawater [msw; hyperbaric oxygenation (HBO) 1.6 atmospheres absolute (ATA)]. On dive 4, before diving, all divers breathed 100% O2 for 20 min at 12 msw (HBO 2.2 ATA). Then they dove to 30 msw (4 ATA) for 20 min breathing air from scuba. After each dive, blood samples were collected as soon as the divers surfaced. Bubbles were measured at 20 and 50 min after decompression and converted to bubble count estimate (BCE) and numeric bubble grade (NBG). BCE and NBG were significantly lower in NBO than in Air [0.142+/-0.034 vs. 0.191+/-0.066 (P<0.05) and 1.61+/-0.25 vs. 1.89+/-0.31 (P<0.05), respectively] at 20 min, but not at 50 min. HBO at 1.6 ATA and 2.2 ATA has a similar significant effect of reducing BCE and NBG. BCE was 0.067+/-0.026 and 0.040+/-0.018 at 20 min and 0.030+/-0.022 and 0.020+/-0.020 at 50 min. NBG was 1.11+/-0.17 and 0.92+/-0.16 at 20 min and 0.83+/-0.18 and 0.75+/-0.16 at 50 min. Prebreathing NBO and HBO significantly alleviated decompression-induced platelet activation. Activation of CD62p was 3.0+/-0.4, 13.5+/-1.3, 10.7+/-0.9, 4.5+/-0.7, and 7.6+/-0.8% for baseline, Air, NBO, HBO at 1.6 ATA, and HBO at 2.2 ATA, respectively. The data show that prebreathing oxygen, more effective with HBO than NBO, decreases air bubbles and platelet activation and, therefore, may be beneficial in reducing the development of decompression sickness.

Evaluation of decompression tables by Doppler technique in caisson work in The Netherlands.

INTRODUCTION: Hyperbaric work was conducted for constructing an underground tramway in the Netherlands. A total of 11,647 exposures were conducted in 41,957 hours. For these working conditions specifically developed oxygen decompression tables were used. METHODS: Fifteen workers were submitted to Doppler monitoring after caisson work at a depth at 12 msw. Measurements were done according to the Canadian DCIEM protocol. For bubble grading the Kisman-Masurel 12-points ordinal scale (0-IV) was used. RESULTS: Bubbles were detected in 17 of the 38 examinations. The highest grade (III-) was found in four measurements. At rest the grading was never higher than I+. Two hours after decompression the grading was remarkably higher than after one hour. CONCLUSIONS: Bubble scores were relatively low, although the maximum grading probably is not reached within two hours after decompression. It may be concluded that the oxygen decompression tables used, were reliable under these heavy working conditions. At group level, decompression stress can be evaluated by Doppler monitoring. In order to reduce health hazard of employees, use of oxygen during decompression in caisson work should be embodied in the occupational standard.

Decompression to altitude: assumptions, experimental evidence, and future directions.

Although differences exist, hypobaric and hyperbaric exposures share common physiological, biochemical, and clinical features, and their comparison may provide further insight into the mechanisms of decompression stress. Although altitude decompression illness (DCI) has been experienced by high-altitude Air Force pilots and is common in ground-based experiments simulating decompression profiles of extravehicular activities (EVAs) or astronauts' space walks, no case has been reported during actual EVAs in the non-weight-bearing microgravity environment of orbital space missions. We are uncertain whether gravity influences decompression outcomes via nitrogen tissue washout or via alterations related to skeletal muscle activity. However, robust experimental evidence demonstrated the role of skeletal muscle exercise, activities, and/or movement in bubble formation and DCI occurrence. Dualism of effects of exercise, positive or negative, on bubble formation and DCI is a striking feature in hypobaric exposure. Therefore, the discussion and the structure of this review are centered on those highlighted unresolved topics about the relationship between muscle activity, decompression, and microgravity. This article also provides, in the context of altitude decompression, an overview of the role of denitrogenation, metabolic gases, gas micronuclei, stabilization of bubbles, biochemical pathways activated by bubbles, nitric oxide, oxygen, anthropometric or physiological variables, Doppler-detectable bubbles, and potential arterialization of bubbles. These findings and uncertainties will produce further physiological challenges to solve in order to line up for the programmed human return to the Moon, the preparation for human exploration of Mars, and the EVAs implementation in a non-zero gravity environment.

Decompression-induced ocular tear film bubbles reflect the process of denitrogenation.

PURPOSE: To confirm that the tear film bubbles observed after decompression from hyperbaric exposure are due to denitrogenation and to assess the time course of denitrogenation based on the number of ocular tear film bubbles. METHODS: The study comprised two parts. In the first, subjects (n = 8) were compressed to a pressure of 2.0 ATA (atmospheres absolute; depth of 10 meters of sea water [msw]) for 60 minutes in a hyperbaric chamber on two separate occasions. On one occasion they breathed air, whereas on the second occasion they inspired pure oxygen. Before and within 30 minutes after each dive, the subjects' tear film was examined with a slit lamp microscope and the average number of bubbles recorded. Ultrasound reflectivity of the lens-vitreous humor compartments was also examined. In the second part of the study, subjects (n = 8) participated in two simulated dives in the hyperbaric chamber: 4.0 ATA (30 msw) for 15 minutes and 2.5 ATA (15 msw) for 180 minutes. The former was a no-stop decompression dive, whereas the latter required a 43-minute decompression stop at 3 msw. Ocular tear film examinations were conducted before the dive, as well as 30 minutes and 1 day, 2 days, and 3 days after the dives. RESULTS: The number of tear film bubbles increased significantly (P < 0.05) after the air dives to 2.0 ATA for 60 minutes, whereas there was no significant postdecompression increase in tear film when oxygen was inspired by the subjects during the dive. Posterior lens-vitreous humor reflectivity increased significantly after decompression from 2 ATA, when air was the breathing mixture, whereas no change in reflectivity was observed when oxygen was inspired during the dive. In the second part of the study, there was a significant elevation in tear film bubbles for 2 days after the two dives (P < 0.05). There was no significant difference in the number of ocular tear film bubbles between the two dives. CONCLUSIONS: After a hyperbaric air exposure, tear film bubbles reflect the process of denitrogenation, which may persist for up to 2 days after the decompression.

Barotrauma and decompression illness of the inner ear: 46 cases during treatment and follow-up.

INTRODUCTION: Diving accidents affecting the inner ear are much more common than was once thought. Among the 319 patients treated in our clinic between January 2002 and November 2005, 46 cases involved 44 divers with symptoms of acute inner ear disorders. The objective of the present article is to investigate the symptoms of the acute disorders and assess any residual damage. STUDY DESIGN: Retrospective case analysis. MATERIALS AND METHODS: The medical records were used to study the cases of 18 divers treated for inner ear decompression illness on 20 occasions and 26 divers who had inner ear barotrauma. The symptoms of the disorder at the beginning of treatment, latency period before the first therapeutic measures, kind of initial therapy, symptoms after the accident, and hearing and balance functions at the last examination in our clinic were assessed. Divers with inner ear decompression illness were examined via means of transcranial or carotid Doppler ultrasonography for the presence of a vascular right-to-left (R/L) shunt. RESULTS: Of 18 divers with inner ear decompression illness, 17 reported vertigo as the main symptom. In one diver, the inner ear decompression illness was manifested bilaterally. The divers with inner ear decompression illness had been treated with hyperbaric oxygen therapy in 14 of 20 cases; the average latency period before the start of therapy was 40 hours (median, 10 h). In 15 (83%) of 18 patients, a large R/L shunt was detected, and in 14 (78%) of 18 patients, residual cochleovestibular damage was detected. Only 9 of 26 patients with inner ear barotrauma mentioned feeling dizzy, and in no patient was vertigo the main symptom. Twenty-one patients complained of tinnitus, whereas 20 complained of hearing loss. The hearing loss ranged from an unobtrusive difference of 10 dB between the ears up to complete deafness. Three patients were subjected to tympanoscopy because of suspected rupture of the round window membrane. Of patients with inner ear barotrauma, 78% had residual cochleovestibular damage. CONCLUSION: We describe for the first time a patient with bilateral manifestation of inner ear decompression illness. Inner ear decompression illness is frequently associated with a R/L shunt; therefore, after a diving accident, the patient's fitness to dive should be assessed via a specialist in diving medicine. Both decompression illness and barotrauma of the inner ear result in residual cochleovestibular damage in more than three of four patients.