Severe Decompression Illness Research Articles

Comparison of treatment recompression tables for neurologic decompression illness in swine model.

BackgroundSignificant reductions in ambient pressure subject an individual to risk of decompression illness (DCI); with incidence up to 35 per 10,000 dives. In severe cases, the central nervous system is often compromised (>80%), making DCI among the most morbid of diving related injuries. While hyperbaric specialists suggest initiating recompression therapy with either a Treatment Table 6 (TT6) or 6A (TT6A), the optimal initial recompression treatment for severe DCI is unknown.MethodsSwine were exposed to an insult dive breathing air at 7.06 ATA (715.35 kPa) for 24 min followed by rapid decompression at a rate of 1.82 ATA/min (184.41 kPa/min). Swine that developed neurologic DCI within 1 hour of surfacing were block randomized to one of four United States Navy Treatment Tables (USN TT): TT6, TT6A-air (21% oxygen, 79% nitrogen), TT6A-nitrox (50% oxygen, 50% nitrogen), and TT6A-heliox (50% oxygen, 50% helium). The primary outcome was the mean number of spinal cord lesions, which was analyzed following cord harvest 24 hours after successful recompression treatment. Secondary outcomes included spinal cord lesion incidence and gross neurologic outcomes based on a pre- and post- modified Tarlov assessment. We compared outcomes among these four groups and between the two treatment profiles (i.e. TT6 and TT6A).ResultsOne-hundred and forty-one swine underwent the insult dive, with 61 swine meeting inclusion criteria (43%). We found no differences in baseline characteristics among the groups. We found no significant differences in functional neurologic outcomes (p = 0.77 and 0.33), spinal cord lesion incidence (p = 0.09 and 0.07), or spinal cord lesion area (p = 0.51 and 0.17) among the four treatment groups or between the two treatment profiles, respectively. While the trends were not statistically significant, animals treated with TT6 had the lowest rates of functional deficits and the fewest spinal cord lesions. Moreover, across all animals, functional neurologic deficit had strong correlation with lesion area pathology (Logistic Regression, p < 0.01, Somers’ D = 0.74).ConclusionsTT6 performed as well as the other treatment tables and is the least resource intensive. TT6 is the most appropriate initial treatment for neurologic DCI in swine, among the tables that we compared.

The effect of the perfluorocarbon emulsion OxycyteTM in an ovine model of severe decompression illness

Background: The treatment of decompression sickness (DCS) with hyperbaric oxygen (HBO2) serves to decrease intravascular bubble size, increase oxygen (O2) delivery to tissue and enhance the elimination of inert gas. Emulsified perfluorocarbons (PFC) combined with breathing O2 have been shown to have similar effects animal models. We studied an ovine model of severe DCS treated with the intravenous PFC OxycyteTM while breathing O2 compared to saline control also breathing O2. Methods: Juvenile male sheep (N=67; weight 24.4+/2.10kg) were compressed to 257 feet of sea water (fsw) in our multiple large-animal chamber where they remained under pressure for 31 minutes. Animals then were decompressed to surface pressure and randomized to receive either Oxycyte at 5mL/kg intravenously (IV) or 5mL/kg saline IV (both receiving 100% O2) 10 minutes after reaching surface pressure. Mortality was recorded at two hours, four hours, and 24 hours after receiving the study drug. Surviving animals underwent perfusion fixation and harvesting of the spinal cord at 24 hours. Spinal cord sections were assessed for volume of lesion area and compared. Results: There was no significant difference in survival at two hours (p=0.2737), four hours (p=0.2101), or 24 hours (p=0.3171). Paralysis at 24 hours was not significantly different. However, spinal cord lesion area was significantly smaller in the Oxycyte group as compared to the saline group, with median spinal cord lesion areas 0.65% vs. 0.94% (p=0.0107). Conclusions: In this ovine model of severe DCS the intravenous PFC Oxycyte did not reduce mortality but did ameliorate spinal cord injury when used after the onset of DCS.

Decompression illness treated at the Geneva hyperbaric facility 2010-2016: A retrospective analysis of local cases.

The Geneva hyperbaric chamber is the main treatment centre for decompression illness (DCI) in Switzerland. The characteristics, symptomatology, treatment and short-term outcome of divers treated at this chamber have not previously been investigated. This was a retrospective study of patients treated with hyperbaric oxygen (HBO) for DCI from 2010 to 2016. Data were analysed to provide a description of the cases and statistical analysis for possible factors associated with an unfavourable outcome. One hundred and thirty-five patients were treated for DCI. Ninety-two were included in the study. Sixty-four presented with neurological and 28 with mild DCI. One hundred and thirty-five patients were treated for DCI. Ninety-two were included in the study. Sixty-four presented with neurological and 28 with mild DCI. Patients with mild DCI mainly had musculoskeletal symptoms (79%). Patients with neurological DCI mainly had spinal (55%), followed by vestibular (36%) symptoms. Arterial gas embolism was diagnosed in 30% of cases. Diving depths ranged between 15 and 142 metres, and dive times between two and 241 min. Median time to treatment was 6 h. Patients with neurological DCI had a high rate (25%) of persisting deficits after treatment. Older age was associated with an unfavourable outcome in univariate but not in multivariate analysis. No adverse effects of HBO were observed. For spinal DCI, a high Boussuges score was associated with persisting deficits after treatment. Our findings are consistent with other series. Severe DCI was associated with a high rate of persisting deficits. No single factor was associated with a negative outcome. A Boussuges score > 7 had sensitivity of 90% and positive predictive value 53% for predicting an unfavourable outcome in spinal DCI.

Case report: Physiological changes due to a rapid ascent from 55 metres underwater.

We present the case of a diver who experienced an uncontrolled ascent from 55 m and presented with a severe decompression illness. She was clinically shocked and in multi organ failure due to massive fluid shifts. She demonstrated bilateral lower limb loss of power and sensation and required multiple hyperbaric therapy sessions. With joint critical care, hyperbaric and physical therapy involvement, she was discharged some five weeks after her presentation with an independent level of function.

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.

Surviving Sepsis Campaign guidelines for a diver with DCI: case report

Severe decompression illness (DCI) is an uncommon medical issue affecting divers and results mainly from rapid surfacing using inadequate decompression protocols. Massive gas embolism with central nervous system involvement often leads to a poor prognosis, with permanent residual neurologic defects. Moreover, DCI complicated with multiple organ dysfunction syndrome (MODS) is tremendously rare and difficult to cure, although hyperbaric oxygen (HBO2) therapy following the U.S. Navy Treatment Tables is a consensus. We report a case of severe DCI with profound shock and MODS after an initial treatment with HBO2 therapy using U.S. Navy Treatment Table 6A. Following the Surviving Sepsis Campaign Guidelines, low-dose hydrocortisone was administered. Although this treatment went against recommendation of the U.S. Navy Diving Manual, it resulted in a dramatic clinical improvement. After a second round of HBO2 treatments, the patient was discharged from hospital two weeks after the diving accident.

Transcatheter closure of patent foramen ovale for the secondary prevention of decompression illness in professional divers: a single-centre experience with long-term follow-up.

Patent foramen ovale (PFO) with occasional right-to-left shunting is associated with an increased risk of decompression illness (DCI). Divers with a history of repetitive or severe DCI and diagnosed with PFO should be considered for transcatheter closure if they wish to continue with unrestricted diving. To summarise our centre's experience in transcatheter PFO closure in professional divers with a history of DCI. A follow-up of 11 consecutive divers (nine males, two females) in whom device PFO closure was performed between 2001 and 2015 was carried out by phone contact. Available medical records and diving logbooks were reviewed to determine individual DCI symptomatology, indications to the procedure, and to evaluate modifications in the diving practice. Each patient experienced at least one event of DCI before the procedure, and eight patients experienced more than one event. Total number of reported events was 62. The vast majority of events (97%) followed dives consistent with safe decompression policies. The median follow-up was 91 (minimum nine, maximum 172) months. No complications of the intervention were observed. All patients returned to unrestricted, deep diving, performing a total of 3610 dives with the median number of 225 dives (lower quartile value: 82.5 dives, upper quartile value: 725 dives). The majority of subjects dived as deep as they did before the intervention, or deeper, achieving mean maximum depth of 93.8 ± 35.6 m (vs. 89.7 ± 25.9 m before the intervention, p = 0.71). No episodes of DCI were reported during the follow-up period. Transcatheter closure of PFO appears to be reasonably effective in secondary prevention of DCI associated with intra-cardiac shunting.

Acute kidney injury caused by decompression illness successfully treated with hyperbaric oxygen therapy and temporary dialysis.

A 52-year-old Japanese male professional diver was referred to our hospital for decompression illness (DCI). After 1h of diving operation at 20m below sea level, he complained of dyspnea, chest pain, and abdominal pain. He dove again, intending to ease the symptoms, but the symptoms were never relieved. He dove for a total of 4h. No neurological abnormalities were observed. Computed tomography images revealed portal venous gas and mesenteric venous gas, in addition to bubbles in the femoral veins, pelvis, lumbar canal, intracranial sinuses, and joints. Hyperbaric oxygen therapy (HBOT) was immediately administered. His symptoms improved after the first course of HBOT, however, the patient had anuria for almost 36h after admission and exhibited acute kidney injury (AKI). Serum creatinine and creatine kinase (CK) levels were increased to maximal values of 6.16 mg/dL and 18,963 U/L, respectively. Blood flow signals were not detected on kidney Doppler ultrasound. We considered that AKI was caused by blood flow impairment and capillary leak syndrome due to DCI in addition to rhabdomyolysis secondary to arterial gas embolism in the skeletal muscles. Temporary dialysis was required to correct the acidemia and electrolyte disturbance. Diuretic phase was initiated, and the patient was put off dialysis on day 3. Serum creatinine and CK levels returned to normal on day 11. He was successfully treated without any complications. Although AKI is a rare manifestation, we should consider AKI risk in patients with severe DCI.

Patent Foramen Ovale Influences the Presentation of Decompression Illness in SCUBA Divers

Few have examined the influence of patent foramen ovale (PFO) on the phenotype of decompression illness (DCI) in affected divers. A retrospective review of our database was performed for 75 SCUBA divers over a 10-year period. 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. 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.

Superior Vestibular Dysfunction in Severe Decompression Sickness Suggests an Embolic Mechanism

Both nitrogen bubble embolism and the difficulty of inner ear tissues to wash out nitrogen have been discussed as possible reasons for the selective vulnerability of the inner ear to decompression illness. This case report suggests that nitrogen bubble embolism plays a crucial role in the pathogenesis of inner ear lesions in decompression accidents. The current patient, a 48-yr-old male dive master, suffered a severe decompression illness with vertigo as the only residual symptom. At the 1-mo follow-up, neuro-otological evaluation revealed a selective lesion of the superior vestibular division of the left labyrinth with normal functioning inferior vestibular division. At vestibular testing, there was no caloric response from the affected left ear, and the head impulse tests for the lateral and anterior semicircular canal were also impaired. Tests of vestibular evoked myogenic potentials (VEMP) showed divergent results. Ocular VEMP in response to left ear stimulation were absent, whereas the cervical VEMP were completely symmetrical and normal. Thus, the lesion profile implies a partial vestibular loss selectively affecting the superior vestibular division of the inner ear. The most likely explanation for such a selective injury seems to be bubble microembolism coupled with both the specific anatomy of this terminally supplied subunit, and with the slow nitrogen wash-out of the vestibular organ.

Decompression Illness Reported in a Survey of 429 Recreational Divers

The purpose of this study was to investigate the influence of diving experience and diving techniques on the lifetime incidence of decompression illness (DCI). Attendants of three diving medical symposia voluntarily answered a questionnaire about their age, gender, medical history, diving experience, diving habits, diving certification levels, and diving associated incidents (cross-sectional survey). Out of 650 divers, 429 completed the questionnaire. The study population consisted of experienced divers with an average of 670 dives. The majority of the divers were certified diving instructors (43%). There were 37 participants (8.7%) who were classified as technical divers with an average of 1193 logged dives. There was an overall lifetime incidence of DCI of 1 per 5463 dives. The complete study group showed an increased lifetime incidence of DCI with decreased diving experience (1.97-fold to 8.17-fold higher). Of the divers, 27% reported severe DCI with neurological symptoms. The lifetime incidence for severe DCI was 1 in 20,291 dives. Again, lifetime incidence for severe DCI was increased with decreased diving certification level (1.1-fold to 13.7-fold higher). Technical divers showed a DCI lifetime incidence of 1 to 8591 dives compared to the non-technical divers with a lifetime incidence of 1 to 5077 dives (not significant). In our study population, the lifetime incidence of DCI was increased in divers with less diving experience. If further studies confirm this finding, diving federations should be encouraged to intensify their efforts of educating divers and should limit diving time and depth in inexperienced divers.

Hyperbare Sauerstofftherapie

Hyperbaric oxygenation (HBO) is a decisive component of a comprehensive interdisciplinary intensive care therapy for numerous disorders, such as gas embolism, severe decompression illness or carbon monoxide (CO) intoxication. However, barochambers with 24 h accessibility are often not readily available, thus, requiring an interhospital transport of critically ill patients. In order to minimise additional risks, a skilled transportation team should be involved. Furthermore, the specific physical and physiological features of HBO require that the transportation personnel must be trained adequately. Specific characteristics of the interhospital transfer of HBO patients are described as well as adverse effects and their specific therapy.

NOS inhibition increases bubble formation and reduces survival in sedentary but not exercised rats.

Previously we have shown that chronic as well as a single bout of exercise 20 h prior to a simulated dive protects rats from severe decompression illness (DCI) and death. However, the mechanism behind this protection is still not known. The present study determines the effect of inhibiting nitric oxide synthase (NOS) on bubble formation in acutely exercised and sedentary rats exposed to hyperbaric pressure. A total of 45 adult female Sprague-Dawley rats (270-320 g) were randomly assigned into exercise or sedentary control groups, with and without NOS inhibition, using L-NAME (0.05 or 1 mg ml(-1)) (a nonselective NOS inhibitor). Exercising rats ran intervals on a treadmill for 1.5 h, 20 h prior to the simulated dive. Intervals alternated between 8 min at 85-90 % of maximal oxygen uptake, and 2 min at 50-60 %. Rats were compressed (simulated dive) in a pressure chamber, at a rate of 200 kPa min(-1) to a pressure of 700 kPa, and maintained for 45 min breathing air. At the end of the exposure period, rats were decompressed linearly to the "surface" (100 kPa) at a rate of 50 kPa min(-1). Immediately after reaching the surface the animals were anaesthetised and the right ventricle was insonated using ultrasound. The study demonstrated that sedentary rats weighing more than 300 g produced a large amount of bubbles, while those weighing less than 300 g produced few bubbles and most survived the protocol. Prior exercise reduced bubble formation and increased survival in rats weighing more than 300 g, confirming the results from the previous study. During NOS inhibition, the simulated dive induced significantly more bubbles in all sedentary rats weighing less than 300 g. However, this effect could be attenuated by a single bout of exercise 20 h before exposure. The present study demonstrates two previously unreported findings: that administration of L-NAME allows substantial bubble formation and decreased survival in sedentary rats, and that a single bout of exercise protects NOS-inhibited rats from severe bubble formation and death. This is the first report to indicate that biochemical processes are involved in bubble formation, and this information may be important in the search for preventive measures for and treatment of DCI.

Recreational scuba diving, patent foramen ovale and their associated risks.

Scuba diving has become a popular leisure time activity with distinct risks to health owing to its physical characteristics. Knowledge of the behaviour of any mixture of breathable gases under increased ambient pressure is crucial for safe diving and gives clues as to the pathophysiology of compression or decompression related disorders. Immersion in cold water augments cardiac pre- and afterload due to an increase of intrathoracic blood volume and peripheral vasoconstriction. In very rare cases, the vasoconstrictor response can lead to pulmonary oedema. Immersion of the face in cold water is associated with bradycardia mediated by increased vagal tone. In icy water, the bradycardia can be so pronounced, that syncope results. For recreational dives, compressed air (i.e., 4 parts nitrogen and 1 part oxygen) is the preferred breathing gas. Its use is limited for diving to 40 to 50 m, otherwise nitrogen narcosis ("rapture of the deep") reduces a diver's cognitive function and increases the risk of inadequate reactions. At depths of 60 to 70 m oxygen toxicity impairs respiration and at higher partial pressures also functioning of the central nervous system. The use of special nitrogen-oxygen mixtures ("nitrox", 60% nitrogen and 40% oxygen as the typical example) decreases the probability of nitrogen narcosis and probably bubble formation, at the cost of increased risk of oxygen toxicity. Most of the health hazards during dives are consequences of changes in gas volume and formation of gas bubbles due to reduction of ambient pressure during a diver's ascent. The term barotrauma encompasses disorders related to over expansion of gas filled body cavities (mainly the lung and the inner ear). Decompression sickness results from the growth of gas nuclei in predominantly fatty tissue. Arterial gas embolism describes the penetration of such gas bubbles into the systemic circulation, either due to pulmonary barotrauma, transpulmonary passage after massive bubble formation ("chokes") or cardiac shunting. In recreational divers, neurological decompression events comprise 80% of reported cases of major decompression problems, most of the time due to pathological effects of intravascular bubbles. In divers with a history of major neurological decompression symptoms without evident cause, transoesophageal echocardiography must be performed to exclude a patent foramen ovale. If a cardiac right-to-left shunt is present, we advise divers with a history of severe decompression illness to stop diving. If they refuse to do so, it is crucial that they change their diving habits, minimising the amount of nitrogen load on the tissue. There is ongoing debate about the long term risk of scuba diving. Neuro-imaging studies revealed an increased frequency of ischaemic brain lesions in divers, which do not correlate well with subtle functional neurological deficits in experienced divers. In the light of the high prevalence of venous gas bubbles even after dives in shallow water and the presence of a cardiac right-to-left shunt in a quarter of the population (i.e., patent foramen ovale), arterialisation of gas bubbles might be more frequent than usually presumed.

Recreational scuba diving, patent foramen ovale and their associated risks.

Scuba diving has become a popular leisure time activity with distinct risks to health owing to its physical characteristics. Knowledge of the behaviour of any mixture of breathable gases under increased ambient pressure is crucial for safe diving and gives clues as to the pathophysiology of compression or decompression related disorders. Immersion in cold water augments cardiac pre- and afterload due to an increase of intrathoracic blood volume and peripheral vasoconstriction. In very rare cases, the vasoconstrictor response can lead to pulmonary oedema. Immersion of the face in cold water is associated with bradycardia mediated by increased vagal tone. In icy water, the bradycardia can be so pronounced, that syncope results. For recreational dives, compressed air (i.e., 4 parts nitrogen and 1 part oxygen) is the preferred breathing gas. Its use is limited for diving to 40 to 50 m, otherwise nitrogen narcosis ("rapture of the deep") reduces a diver's cognitive function and increases the risk of inadequate reactions. At depths of 60 to 70 m oxygen toxicity impairs respiration and at higher partial pressures also functioning of the central nervous system. The use of special nitrogen-oxygen mixtures ("nitrox", 60% nitrogen and 40% oxygen as the typical example) decreases the probability of nitrogen narcosis and probably bubble formation, at the cost of increased risk of oxygen toxicity. Most of the health hazards during dives are consequences of changes in gas volume and formation of gas bubbles due to reduction of ambient pressure during a diver's ascent. The term barotrauma encompasses disorders related to over expansion of gas filled body cavities (mainly the lung and the inner ear). Decompression sickness results from the growth of gas nuclei in predominantly fatty tissue. Arterial gas embolism describes the penetration of such gas bubbles into the systemic circulation, either due to pulmonary barotrauma, transpulmonary passage after massive bubble formation ("chokes") or cardiac shunting. In recreational divers, neurological decompression events comprise 80% of reported cases of major decompression problems, most of the time due to pathological effects of intravascular bubbles. In divers with a history of major neurological decompression symptoms without evident cause, transoesophageal echocardiography must be performed to exclude a patent foramen ovale. If a cardiac right-to-left shunt is present, we advise divers with a history of severe decompression illness to stop diving. If they refuse to do so, it is crucial that they change their diving habits, minimising the amount of nitrogen load on the tissue. There is ongoing debate about the long term risk of scuba diving. Neuro-imaging studies revealed an increased frequency of ischaemic brain lesions in divers, which do not correlate well with subtle functional neurological deficits in experienced divers. In the light of the high prevalence of venous gas bubbles even after dives in shallow water and the presence of a cardiac right-to-left shunt in a quarter of the population (i.e., patent foramen ovale), arterialisation of gas bubbles might be more frequent than usually presumed.

Syndrome de détresse respiratoire aiguë après oxygénothérapie hyperbare prolongée : un cas d’intoxication pulmonaire à l’oxygène ?

A 42-year-old patient was admitted to our ICU for severe decompression illness with tetraplegia. He presented an acute respiratory distress syndrome (ARDS), following a very long hyperbaric oxygen therapy (using a US. Navy Treatment Table 7). The ARDS resulted in pulmonary fibrosis, and the patient died despite maximal support in ICU. The risk of pulmonary toxicity of oxygen must be considered when using a prolonged recompression treatment table.

Intravenous Lidocaine as Adjunctive Therapy in the Treatment of Decompression Illness

Two cases of severe decompression illness for which IV lidocaine was used as adjunctive therapy to recompression and hyperbaric oxygen therapy are described. The first patient demonstrated improvement only after lidocaine was added to her treatment; the second had essentially complete recovery after only a single treatment despite severe symptoms and a significant delay in presentation. These cases support the need for a controlled clinical trial of lidocaine as an adjunct to hyperbaric therapy in decompression illness. [Cogar WB: Intravenous lidocaine as adjunctive therapy in the treatment of decompression illness. Ann Emerg Med February 1997;29:284-286.]