Patent Foramen Ovale Closure and Decompression Sickness Among Divers

BackgroundDecompression sickness is a diving-related disease that results in various clinical manifestations, ranging from joint pain to severe pulmonary and CNS affection. Complications of this disease may sometimes persist even after treatment with hyperbaric oxygen therapy. In addition, it may hamper the quality of life by forcing divers to restrict their recreational practice. The presence of a patent foramen ovale (PFO) increases the risk of decompression sickness by facilitating air embolization. Therefore, PFO closure may play a role in reducing such complications. However, PFO closure remains associated with its own set of risks and complications. We sought to assess the benefit and harm of PFO closure for the prevention of decompression sickness in divers.MethodsWe conducted a comprehensive search of MEDLINE, Embase, CENTRAL, and Web of Science. Two-armed studies comparing the incidence of decompression sickness with or without PFO closure were included. We used a random-effects model to compute risk ratios comparing groups undergoing PFO closure to those not undergoing PFO closure.ResultsFour observational studies with a total of 309 divers (PFO closure: 141 and no closure: 168) met inclusion criteria. PFO closure was associated with a significantly lower incidence of decompression sickness (PFO-closure: 2.84%; no closure: 11.3%; RR: 0.29; 95% CI: 0.10 to 0.89; NNTB = 11), with low heterogeneity (I² = 0%). The mean follow-up was 6.12 years (Standard deviation 0.70). Adverse events occurred in 7.63% of PFO closures, including tachyarrhythmias and bleeding.ConclusionPFO closure may potentially reduce the risk of decompression sickness among divers; however, it is not free of potential downsides, with nearly one in thirteen patients in our analysis experiencing an adverse event.     

Diving up to 60 m depth followed by decompression has no effect on pro-enzyme and total thrombin activatable fibrinolysis inhibitor antigen concentration.

The aim of our study was to investigate the effect of two different hyperbaric exposures followed by decompression on thrombin activatable fibrinolysis inhibitor (TAFI) concentration and activity. The hyperbaric conditions correspond to diving to 30 and 60 m water depth. Thirty-four male divers were tested in decompression habitat LSH-200, with air as a breathing medium. The pro-enzyme and total TAFI antigen concentration were measured. We did not observed significant changes of either pro-enzyme or total TAFI antigen concentration after both series of exposures followed by decompression. The results may suggest that TAFI plays only a marginal role, if any, in the regulation of induced fibrinolysis in divers, which may contribute to bleeding episodes in a course of decompression sickness.     

Early detection of asymptomatic dysbaric osteonecrosis of the shoulder after type 1 decompression sickness: a case report

INTRODUCTION: Dysbaric osteonecrosis is a rare illness in professional divers and compressed-air workers. The correlation between dysbaric osteonecrosis and previous decompression sickness with osteoarthromuscular pain (type 1 decompression sickness) remains a controversial subject. The probability for ischemic lesions detected with MRI to turn into osteonecrosis after decompression sickness is still not established. EXEGESIS: The authors report the case of a military diver declared definitely medically unfit to dive after the occurrence of advanced dysbaric osteonecrosis of the shoulder, eight months after decompression sickness treated with hyperbaric oxygen, in the same area. A close link between those two events and the requirement for monitoring the follow-up of acute type 1 decompression sickness are discussed. CONCLUSION: Every decompression sickness with osteoarthromuscular pain should be early examined with MRI in order to screen osteomedullar damages liable to worse with diving and change subsequently in bone necrosis.     

Evidence for increasing patency of the foramen ovale in divers

Using a standardized contrast-enhanced transesophageal echocardiographic technique, a group of divers was reexamined for the presence and size of patent foramen ovale (PFO) 7 years after their initial examinations. Unexpected but significant increases in the prevalence and size of PFO were found, suggesting a possible increasing risk for decompression sickness in these divers over time.     

Bilateral massive pulmonary embolism secondary to decompression sickness: a case report

This case report describes massive pulmonary embolism in a patient as a complication of decompression illness. Twenty-four hours after a scuba dive, a 50-year-old man developed acute pulmonary hypertension and decompression sickness that produced bilateral embolism in the lung at day 6 of hospitalization. He had no risk factor for pulmonary embolism earlier except smoking. Decompression sickness that RESULTS in formation of bubbles of inert gas is a risk for both aviators and divers. The present case strongly suggests that micro-bubbles may cause life-threatening massive pulmonary embolism.     

Physiological and clinical aspects of apnea diving

Apnea diving is a fascinating example of applied physiology. The record for apnea diving as an extreme sport is 171 meters, 8:58 minutes. The short time beneath the surface induces profound cardiovascular and respiratory effects. Variations of blood-gas tensions result from the interaction of metabolism and the rapid sequence of compression and decompression. Decompression sickness is possible. Apnea divers can reach depths beyond the theoretic physiologic limit by using the lung-packing maneuver. Apnea divers exhibit a fall in heart rate, which can be trained and is an oxygen-conserving effect, but increases the incidence of ventricular arrhythmia.     

Patent foramen ovale: a review of associated conditions and the impact of physiological size

Patent foramen ovale (PFO) is implicated in platypnea-orthodeoxia, stroke and decompression sickness (DCS) in divers and astronauts. However, PFO size in relation to clinical illness is largely unknown since few studies evaluate PFO, either functionally or anatomically. The autopsy incidence of PFO is approximately 27% and 6% for a large defect (0.6 cm to 1.0 cm). A PFO is often associated with atrial septal aneurysm and Chiari network, although these anatomic variations are uncommon. Methodologies for diagnosis and anatomic and functional sizing of a PFO include transthoracic echocardiography (TTE), transesophageal echocardiography (TEE) and transcranial Doppler (TCD), with saline contrast. Saline injection via the right femoral vein appears to have a higher diagnostic yield for PFO than via the right antecubital vein. Saline contrast with TTE using native tissue harmonics or transmitral pulsed wave Doppler have quantitated PFO functional size, while TEE is presently the reference standard. The platypnea-orthodeoxia syndrome is associated with a large resting PFO shunt. Transthoracic echocardiography, TEE and TCD have been used in an attempt to quantitate PFO in patients with cryptogenic stroke. The larger PFOs (approximately > or =4 mm size) or those with significant resting shunts appear to be clinically significant. Approximately two-thirds of divers with unexplained DCS have a PFO that may be responsible and may be related to PFO size. Limited data are available on the incidence of PFO in high altitude aviators with DCS, but there appears to be a relationship. A large decompression stress is associated with extra vehicular activity (EVA) from spacecraft. After four cases of serious DCS in EVA simulations, a resting PFO was detected by contrast TTE in three cases. Patent foramen ovales vary in both anatomical and functional size, and the clinical impact of a particular PFO in various situations (platypnea-orthodeoxia, thromboembolism, DCS in underwater divers, DCS in high-altitude aviators and astronauts) may be different.     

Screening and Risk Stratification Strategy Reduced Decompression Sickness Occurrence in Divers With Patent Foramen Ovale

ObjectivesThis paper sought to evaluate the occurrence of decompression sickness (DCS) after the application of a patent foramen ovale (PFO) screening and risk stratification strategy.BackgroundPFO is associated with an increased risk of DCS. Recently, transcatheter closure was reported to reduce DCS occurrence in divers with a high-grade shunt. However, to date, there are no data regarding the effectiveness of any PFO screening and risk stratification strategy for divers.MethodsA total of 829 consecutive divers (age 35.4 ± 10.0 years, 81.5% men) were screened for PFO by means of transcranial color-coded sonography in the DIVE-PFO (Decompression Illness Prevention in Divers with a Patent Foramen Ovale) registry. Divers with a high-grade PFO were offered either catheter-based PFO closure (the closure group) or advised conservative diving (high grades). Divers with a low-grade shunt were advised conservative diving (low grades), whereas those with no PFO continued unrestricted diving (controls). A telephone follow-up was performed. To study the effect of the screening and risk stratification strategy, DCS occurrence before enrollment and during the follow-up was compared.ResultsFollow-up was available for 748 (90%) divers. Seven hundred and 2 divers continued diving and were included in the analysis (mean follow-up 6.5 ± 3.5 years). The DCS incidence decreased significantly in all groups, except the controls. During follow-up, there were no DCS events in the closure group; DCS incidence was similar to the controls in the low-grade group (HR: 3.965; 95% CI: 0.558-28.18; P = 0.169) but remained higher in the high-grade group (HR: 26.170; 95% CI: 5.797-118.160; P < 0.0001).ConclusionsThe screening and risk stratification strategy using transcranial color-coded sonography was associated with a decrease in DCS occurrence in divers with PFO. Catheter-based PFO closure was associated with a DCS occurrence similar to the controls; the conservative strategy had a similar effect in the low-grade group, but in the high-grade group the DCS incidence remained higher than in all other groups.     

Patent foramen ovale: an underrated risk for divers?

The foramen ovale which is the fetal connection between the right and left atrium persists in about 30 % of the adult population. In the presence of a persistent foramen ovale (PFO) shunting of blood may occur from the right to the left atrium, and bubbles can reach the systemic circulation during or after the decompression phase of a dive with compressed air. Therefore, divers with PFO may have an increased risk to develop ischemic cerebral lesions and neurologic decompression sickness (DCS). Significant right-to-left shunting may be diagnosed using transcranial doppler ultrasound of the medial cerebral artery and echocardiography with echo contrast media and Valsalva provocation. However, there are no official guidelines concerning PFO screening in medical fitness exams for professional or recreational divers in Germany. Therefore, it remains in the diver's choice to be screened for PFO. Divers with a history of DCS should be monitored for PFO, especially when diving strictly adhered to decompression tables. Divers with PFO who refuse to stop diving after DCS should be advised to adhere to very save dive profiles.     

Risk of decompression illness among 230 divers in relation to the presence and size of patent foramen ovale.

BACKGROUND: The risk of developing decompression illness (DCI) in divers with a patent foramen ovale (PFO) has not been directly determined so far; neither has it been assessed in relation to the PFO's size. METHODS: In 230 scuba divers (age 39+/-8 years), contrast trans-oesophageal echocardiography (TEE) was performed for the detection and size grading (0-3) of PFO. Prior to TEE, the study individuals answered a detailed questionnaire about their health status and about their diving habits and accidents. For inclusion into the study, > or =200 dives and strict adherence to decompression tables were required. RESULTS: Sixty-three divers (27%) had a PFO. Overall, the absolute risk of suffering a DCI event was 2.5 per 10(4) dives. There were 18 divers (29%) with, and 10 divers (6%) without, PFO who had experienced > or =1 major DCI events P=0.016. In the group with PFO, the incidence per 10(4) dives of a major DCI, a DCI lasting longer than 24 h and of being treated in a decompression chamber amounted to 5.1 (median 0, interquartile range [IQR] 0-10.0), 1.9 (median 0, IQR 0-4.0) and 3.6 (median 0, IQR 0-9.8), respectively and was 4.8-12.9-fold higher than in the group without PFO (P<0.001). The risk of suffering a major DCI, of a DCI lasting longer than 24 h and of being treated by recompression increased with rising PFO size. CONCLUSION: The presence of a PFO is related to a low absolute risk of suffering five major DCI events per 10(4) dives, the odds of which is five times as high as in divers without PFO. The risk of suffering a major DCI parallels PFO size.     

Dysbaric cerebral air embolism in Hawaii

Cerebral air embolism is a major cause of death and disability among sport scuba divers. To better define the epidemiologic and clinical manifestations of this infrequently encountered disorder, the records of all recompression treatments in Hawaii from 1976 through 1979 were reviewed. Forty-two cases of dysbaric air embolism (DAE) were identified on the basis of clinical criteria, accounting for 18% of the patients undergoing recompression treatment for diving-related disorders during this four-year period. In 22 patients (52%), DAE was part of a dysbarism syndrome that involved one or more forms of decompression sickness and/or in which DAE could not be differentiated from neurologic decompression sickness. The presenting signs and symptoms varied, with asymmetric multiplegia being the most common finding. Two patients died, giving a case fatality rate of 5% for those who survived until reaching the recompression chamber. Overall, 78% of the cases manifested either complete (61%) or substantial (17%) recovery with recompression and adjunctive medical measures. Traditional concepts of dysbaric cerebral air embolism are not adequate to explain the spectrum of clinical manifestations encountered in this condition.     

Decompression illness

Decompression illness is caused by intravascular or extravascular bubbles that are formed as a result of reduction in environmental pressure (decompression). The term covers both arterial gas embolism, in which alveolar gas or venous gas emboli (via cardiac shunts or via pulmonary vessels) are introduced into the arterial circulation, and decompression sickness, which is caused by in-situ bubble formation from dissolved inert gas. Both syndromes can occur in divers, compressed air workers, aviators, and astronauts, but arterial gas embolism also arises from iatrogenic causes unrelated to decompression. Risk of decompression illness is affected by immersion, exercise, and heat or cold. Manifestations range from itching and minor pain to neurological symptoms, cardiac collapse, and death. First-aid treatment is 100% oxygen and definitive treatment is recompression to increased pressure, breathing 100% oxygen. Adjunctive treatment, including fluid administration and prophylaxis against venous thromboembolism in paralysed patients, is also recommended. Treatment is, in most cases, effective although residual deficits can remain in serious cases, even after several recompressions.     

Other modalities of oxygen therapy: hyperbaric oxygen, nitric oxide, and ECMO

Novel therapies for the next decade include hyperbaric oxygen, nitric oxide, and extracorporeal membrane oxygenation. Hyperbaric oxygen delivers oxygen at a pressure greater than one atmosphere and has been used in diseases ranging from decompression sickness to carbon monoxide poisoning. Inhaled nitric oxide, a potent vasodilator, has been used in the acute respiratory distress syndrome and for the diagnosis and treatment of pulmonary hypertension. Extracorporeal membrane oxygenation (ECMO) has been used to provide cardiopulmonary bypass support, particularly in the pediatric and neonatal population.     

A mystery featuring right-to-left shunting despite normal intracardiac pressure

The cause of right-to-left atrial shunting despite normal intracardiac pressures and normal or near-normal pulmonary function through a patent foramen ovale has still not been completely clarified. It is probably responsible for several linked diseases, such as paradoxical embolism, platypnea-orthodeoxia syndrome, migraine with aura, transient global amnesia, and decompression sickness in sport divers. Despite modern diagnostic methods, the underlying anatomophysiologic and pathogenic mechanisms of right-to-left atrial shunting without abnormal intracardiac pressures remain a matter of debate and controversy. Holistically speaking, a return to a direct study of embryology, gross anatomy, and physiology may help us elucidate the real mechanism of this paradoxical shunting.     

Vasopressin dysregulation: hyponatremia, fluid retention and congestive heart failure

Patent foramen ovale is a frequent remnant of the fetal circulation. Affecting approximately 25% of the adult population. Its recognition, evaluation and treatment has attracted increasing interest as the importance and frequency of its implication in several pathologic processes, including ischemic stroke secondary to paradoxic embolism, the platypnea-orthodeoxia syndrome, decompression sickness (DCS) (an occupational hazard for underwater divers and high altitude aviators and astronauts) and migraine headache, has become better understood. Echocardiographic techniques have emerged as the principle means for diagnosis and assessment of PFO, in particular contrast echocardiography and transcranial Doppler. Its treatment remains controversial with a general tendency to propose a percutaneous closure among the symptomatic patients.     

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.     

高空减压病在航空医学中的防治新进展

高空减压病（altitude decompression sickness,ADS）是指在一定高度飞行时,大气压力迅速降低,原本溶解在机体组织与体液中的氮气呈现过饱和状态而离析出来形成气泡,压迫或栓塞局部组织产生的一种病症。ADS是一种比较常见的航空病,高空低气压的暴露使飞行人员面临着ADS的风险,在过去很长的一段时间,国内外学者针对ADS的病因、预防以及治疗做了大量工作,取得了大量的突破性进展,但近年来随着航空器性能的不断提升,ADS的防治又面临新的挑战,本文将对近年来国内外ADS的发病原因、治疗以及预防新进展做一综述。     

Progressive ulnar palsy as a late complication of decompression sickness

We report an unusual case of decompression sickness in which a progressive ulnar palsy developed 22 days after the onset of neurological decompression sickness. The initial symptoms of numbness and paresthesias of the hand were treated with recompression therapy, resulting in only partial relief. The patient subsequently developed weakness of the left hand, which increased in severity until the institution of repeated daily hyperbaric oxygen treatments. A total of seven treatments resulted in partial resolution of the patient's signs and symptoms. Recovery was complete within four months.     

Relation between directly detected patent foramen ovale and ischemic brain lesions in sport divers

BACKGROUND: In divers, the significance of a patent foramen ovale and its potential relation to paradoxical gas emboli remain uncertain. OBJECTIVE: To assess the prevalence of symptoms of decompression illness and ischemic brain lesions in divers with regard to the presence of a patent foramen ovale. DESIGN: Retrospective cohort study. SETTING: University hospital and three diving clubs in Switzerland. PARTICIPANTS: 52 sport divers and 52 nondiving controls. MEASUREMENTS: Prevalence of self-reported decompression events, patent foramen ovale on contrast transesophageal echocardiography, and ischemic brain lesions on magnetic resonance imaging. RESULTS: The risk for decompression illness events was 4.5-fold greater in divers with patent foramen ovale than in divers without patent foramen ovale (risk ratio, 4.5 [95% CI, 1.2 to 18.0]; P = 0.03). Among divers, 1.23 +/- 2.0 and 0.64 +/- 1.22 ischemic brain lesions per person (mean +/- SD) were detected in those with and those without patent foramen ovale, respectively. Among controls, 0.22 +/- 0.44 and 0.12 +/- 0.63 lesion per person were detected (P < 0.001 for all groups). CONCLUSIONS: Regardless of whether a diver has a patent foramen ovale, diving is associated with ischemic brain lesions.     

Bone and joint lesions in decompression sickness

1 Of 450 divers, 268 (59.5%) has aseptic necrosis of bone; 81 had articular lesions. 2 In proportion to duration of diving experience and maximum depth of diving, incidence of bone necrosis increases. 3 The radiological lesions have been classified by modified Ohta-Matsunaga criteria. 4 Yearly progress of bone changes were mentioned. 5 Pathological appearances of aseptic necrosis of bone in divers are compared with different types of bone necrosis. 6 Experimental studies for aseptic necrosis were mentioned. 7 Etiology of bone necrosis is not yet clear, but some etiological factors were discussed. It was suggested that fat embolism was an important factor, because fat embolisms were seen in our pathological findings of the divers and compressed-air workers. 8 Periodic radiological examination of the bones of divers and compressed-air workers should be carried out. It is important to research the new modified decompression table to prevent bone necrosis. 9 Surgical treatment of bone necrosis was mentioned.