Transesophageal echocardiography detection of air embolism during endoscopic surgery and validity of hyperbaric oxygen therapy: Case report.

INTRODUCTION: Air embolism has the potential to be serious and fatal. In this paper, we report 3 cases of air embolism associated with endoscopic medical procedures in which the patients were treated with hyperbaric oxygen immediately after diagnosis by transesophageal echocardiography. In addition, we systematically review the risk factors for air embolism, clinical presentation, treatment, and the importance of early hyperbaric oxygen therapy efficacy after recognition of air embolism. PATIENT CONCERNS: We present 3 patients with varying degrees of air embolism during endoscopic procedures, one of which was fatal, with large amounts of gas visible in the right and left heart chambers and pulmonary artery, 1 showing right heart enlargement with increased pulmonary artery pressure and tricuspid regurgitation, and 1 showing only a small amount of gas images in the heart chambers. DIAGNOSES: Based on ETCO2 and transesophageal echocardiography (TEE), diagnoses of air embolism were made. INTERVENTIONS: The patients received symptomatic supportive therapy including CPR, 100% O2 ventilation, cerebral protection, hyperbaric oxygen therapy and rehabilitation. OUTCOMES: Air embolism can causes respiratory, circulatory and neurological dysfunction. After aggressive treatment, one of the 3 patients died, 1 had permanent visual impairment, and 1 recovered completely without comorbidities. CONCLUSIONS: While it is common for small amounts of air/air bubbles to enter the circulatory system during endoscopic procedures, life-threatening air embolism is rare. Air embolism can lead to serious consequences, including respiratory, circulatory, and neurological impairment. Therefore, early recognition of severe air embolism and prompt hyperbaric oxygen therapy are essential to avoid its serious complications.

Cerebral Air Embolism after Esophagogastroduodenoscopy: Insight on Pathophysiology, Epidemiology, Prevention and Treatment.

BACKGROUND: Air embolism is an extremely rare complication that can follow gastrointestinal endoscopy. The most accepted treatment of cerebral air embolism (CAE) is hyperbaric oxygen (HBO). Limited evidence suggests that lidocaine may have a neuroprotective effect. The exact mechanism does not appear to be well elucidated. METHODS: We conducted a literature search using multiple combinations of keywords from PubMed and Ovid Medline databases according to the PRISMA guidelines. We included articles with cases of air embolism caused by an esophagogastroduodenoscopy (EGD). We excluded cases related to other procedures e.g. colonoscopy, endoscopic retrograde cholangiopancreatography, cholangioscopy, Kasai procedure, bronchoscopy, laparoscopy or thoracoscopy. We were able to identify 30 cases of CAE associated with EGD. We included our experience in treating one patient with CAE after elective EGD. RESULTS: Given the results of our literature search and this patient's characteristics, we chose to treat our patient with HBO and lidocaine infusion. Our case series consists of 31 patients of post EGD CAE, the mean age was 63.7 ± 11.14 years, 38.7% of the patients were women (n = 12). 38.7% of the cases underwent esophageal dilatation (n = 12), while 19.35% had EGD biopsy (n = 6), 9.6% had variceal ligation (n = 3), and 3.22% had variceal banding (n = 1). In 20 out of 31 cases, echocardiography has been documented, 20% of those patients (n = 4) had patent foramen ovale. HBO was used in treatment of 48% of cases (n = 15), among the included patients, 61% survived (n = 19). Our patient showed significant neurological improvement. CONCLUSIONS: Despite the rare incidence of CAE during or after EGD, physicians should be aware of this potential complication. In patients who develop sudden acute neurological symptoms, early diagnosis and intervention may prevent devastating neurological injury and death. The most accepted emergent treatment for CAE includes HBO, consideration of lidocaine, and work-up of source of the air embolism.

Medical Management and Risk Reduction of the Cardiovascular Effects of Underwater Diving.

Undersea diving is a sport and commercial industry. Knowledge of potential problems began with Caisson disease or "the bends", first identified with compressed air in the construction of tunnels under rivers in the 19th century. Subsequently, there was the commercially used old-fashioned diving helmet attached to a suit, with compressed air pumped down from the surface. Breathhold diving, with no supplementary source of air or other breathing mixture, is also a sport as well as a commercial fishing tool in some parts of the world. There has been an evolution to self-contained underwater breathing apparatus (SCUBA) diving with major involvement as a recreational sport but also of major commercial importance. Knowledge of the physiology and cardiovascular plus other medical problems associated with the various forms of diving have evolved extensively. The major medical catastrophes of SCUBA diving are air embolism and decompression sickness (DCS). Understanding of the essential referral to a hyperbaric recompression chamber for these problems is critical, as well as immediate measures until that recompression is achieved. These include the administration of 100% oxygen and rehydration with intravenous normal saline. Undersea diving continues to expand, especially as a sport, and a basic understanding of the associated preventive and emergency medicine will decrease complications and save lives.

Updates in Decompression Illness.

Decompression sickness and arterial gas embolism, collectively known as decompression illness (DCI), are rare but serious afflictions that can result from compressed gas diving exposures. Risk is primarily determined by the pressure-time profile but is influenced by several factors. DCI can present idiosyncratically but with a wide range of neurologic symptoms. Examination is critical for assessment in the absence of diagnostic indicators. Many conditions must be considered in the differential diagnosis. High-fraction oxygen breathing provides first aid but definitive treatment of DCI is hyperbaric oxygen.

Effect of metabolic gases and water vapor, perfluorocarbon emulsions, and nitric oxide on tissue bubbles during decompression sickness.

In aviation and diving, fast decrease in ambient pressure, such as during accidental loss of cabin pressure or when a diver decompresses too fast to sea level, may cause nitrogen (N2) bubble formation in blood and tissue resulting in decompression sickness (DCS). Conventional treatment of DCS is oxygen (O2) breathing combined with recompression.  However, bubble kinetic models suggest, that metabolic gases, i.e. O2 and carbon dioxide (CO2), and water vapor contribute significantly to DCS bubble volume and growth at hypobaric altitude exposures. Further, perfluorocarbon emulsions (PFC) and nitric oxide (NO) donors have, on an experimental basis, demonstrated therapeutic properties both as treatment and prophylactic intervention against DCS. The effect was ascribed to solubility of respiratory gases in PFC, plausible NO elicited nuclei demise and/or N2 washout through enhanced blood flow rate. Accordingly, by means of monitoring injected bubbles in exposed adipose tissue or measurements of spinal evoked potentials (SEPs) in anaesthetized rats, the aim of this study was to: 1) evaluate the contribution of metabolic gases and water vapor to bubble volume at different barometrical altitude exposures, 2) clarify the O2 contribution and N2 solubility from bubbles during administration of PFC at normo- and hypobaric conditions and, 3) test the effect of different NO donors on SEPs during DCS upon a hyperbaric air dive and, to study the influence of  NO on tissue bubbles at high altitude exposures. The results support the bubble kinetic models and indicate that metabolic gases and water vapor contribute significantly to bubble volume at 25 kPa (~10,376 m above sea level) and constitute a threshold for bubble stabilization or decay at the interval of 47-36 kPa (~6,036 and ~7,920 m above sea level). The effect of the metabolic gases and water vapor seemed to compromise the therapeutic properties of both PFC and NO at altitude, while PFC significantly increased bubble disappearance rate at sea level following a hyperbaric airdive. We found no protective effect of NO donors during DCS from diving. On the contrary, there was a tendency towards a poorer outcome when decompression was combined with NO donor administration. This observation is seemingly contradictive to recent publications and may be explained by the multifactorial effect of NO in combination with a fast decompression profile, speeding up the N2 release from tissues and thereby aggravating the DCS symptoms.

Hyperbaric oxygen does not improve cerebral function when started 2 or 4 hours after cerebral arterial gas embolism in swine.

OBJECTIVE: Hyperbaric oxygenation is the accepted treatment for cerebral arterial gas embolism. Although earlier start of hyperbaric oxygenation is associated with better outcome, it is unknown how much delay can be tolerated before start of hyperbaric oxygenation. This study investigates the effect of hyperbaric oxygenation on cerebral function in swine when initiated 2 or 4 hours after cerebral arterial gas embolism. DESIGN: Prospective interventional animal study. SETTING: Surgical laboratory and hyperbaric chamber. SUBJECTS: Twenty-two Landrace pigs. INTERVENTIONS: Under general anesthesia, probes to measure intracranial pressure, brain oxygen tension (PbtO2), and brain microdialysis, and electrodes for electroencephalography were placed. The electroencephalogram (quantified using temporal brain symmetry index) was suppressed during 1 hour by repeated injection of air boluses through a catheter placed in the right ascending pharyngeal artery. Hyperbaric oxygenation was administered using U.S. Navy Treatment Table 6 after 2- or 4-hour delay. Control animals were maintained on an inspiratory oxygen fraction of 0.4. MEASUREMENTS AND MAIN RESULTS: Intracranial pressure increased to a mean maximum of 19 mm Hg (SD, 4.5 mm Hg) due to the embolization procedure. Hyperbaric oxygenation significantly increased PbtO2 in both groups treated with hyperbaric oxygenation (mean maximum PbtO2, 390 torr; SD, 177 torr). There were no significant differences between groups with regard to temporal brain symmetry index (control vs 2-hr delay, p = 0.078; control vs 4-hr delay, p = 0.150), intracranial pressure, and microdialysis values. CONCLUSIONS: We did not observe an effect of hyperbaric oxygenation on cerebral function after a delay of 2 or 4 hours. The injury caused in our model could be too severe for a single session of hyperbaric oxygenation to be effective. Our study should not change current hyperbaric oxygenation strategies for cerebral arterial gas embolism, but further research is necessary to elucidate our results. Whether less severe injury benefits from hyperbaric oxygenation should be investigated in models using smaller amounts of air and clinical outcome measures.

Electrocardiogram and X-ray findings associated with iatrogenic pulmonary venous gas embolism.

Iatrogenic venous gas embolism (VGE) has been described in cases of patients with hemodialysis catheters and other thoracic central lines. When VGE is present, it may lead to large gas bubbles in the right heart or pulmonary circulation. We reviewed a case of a 52-year-old male hemodialysis patient who inadvertently received an unknown amount of air through a faulty connection in his line during hemodialysis treatment. The patient was symptomatic with chest pain and was found to have an ECG indicative of acute right heart strain and an unusual bulging of his right mediastinum on X-ray. An emergency consult was called for hyperbaric oxygen therapy (HBO2T) due to the known indications for therapy. The patient had a full recovery after HBO2T and had complete relief of his chest pain after compression. Repeat decubitus chest X-ray and ECG post-HBO2T showed resolution of the mediastinal bulge, and ECG had reverted to the patient's baseline tracing. Iatrogenic pulmonary VGE may be diagnosed with the aid of ECG and X-ray findings when correlated with historical and other clinical elements. HBO2 treatment success may be correlated with reversal of ECG and X-ray findings in patients with clinical improvement.

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.

Perfluorocarbon emulsions as a promising technology: a review of tissue and vascular gas dynamics.

Perfluorocarbon (PFC) emulsions are halogen-substituted carbon nonpolar oils with resultant enhanced dissolved respiratory gas (O(2), N(2), CO(2), nitric oxide) capabilities. In the first demonstration of enhanced O(2) solubility, inhaled PFC could sustain rat metabolism. Intravenous emulsions were then trialed as "blood substitutes." In the last 10 yr, biocomputational modeling has enhanced our mechanistic understanding of PFCs. Contemporary research is now taking advantage of these physiological discoveries and applying PFCs as "oxygen therapeutics," as well as ways to enhance other gas movements. One particularly promising area of research is the treatment of gas embolism (arterial and venous emboli/decompression sickness). An expansive understanding of PFC-enhanced diffusive gas movements through tissue and vasculature may have analogous applications for O(2) or other respiratory gases and should provide a revolution in medicine. This review will stress the fundamental knowledge we now have regarding how respiratory gas movements are changed when intravenous PFC is present.

Retrograde cerebral perfusion and delayed hyperbaric oxygen for massive air embolism during cardiac surgery.

We report a case of massive air embolism from a ventricular vent line during cardiac surgery successfully treated with emergent retrograde cerebral perfusion and delayed hyperbaric oxygen therapy. The etiologies of this rare but potentially devastating complication are discussed along with prevention and treatment options.

Accidental cerebral venous gas embolism in a young patient with congenital heart disease.

This article describes an 11-year-old girl with a diagnosis of Ebstein's anomaly. Glenn and Fontan surgeries were performed successfully. She had a generalized tonic-clonic seizure after peripheral intravenous infusion under pressure. A computed tomography brain scan performed 30 minutes later showed multiple serpiginous hypodensities in the cortical sulci and in the superior longitudinal sinus compatible with cerebral venous gas embolism. At follow-up 1 month later, the girl had severe motor impairment. Cerebral gas embolism should be considered in a patient with risk factors and acute neurological symptoms in order to select the treatment of choice, hyperbaric oxygen, and reduce damage to brain tissues.

HBO and gas embolism.

Gas embolism, which occurs with the entry of gas into the circulatory system from the vein, artery or both, is a potentially serious even fatal condition. The two main causes of gas embolism are iatrogenic and diving. The site of entry and the signs and symptoms distinguish between arterial and venous embolism. The entering gas may be air, but may also be CO(2) or other gases, especially in iatrogenic embolism. Supportive care is the primary therapy for venous gas embolism, while hyperbaric oxygen therapy in addition to supportive care is the first line of treatment for arterial gas embolism. In this article, we will review the pathophysiology, etiology, diagnosis and treatment of gas embolism.

Increased expired NO and roles of CO2 and endogenous NO after venous gas embolism in rabbits.

Venous gas embolism (VGE) is a feared complication in diving, aviation, surgery and trauma. We hypothesized that air emboli in the lung circulation might change expired nitric oxide (FeNO). A single intravenous infusion of air was given (100 mul kg(-1)) to three groups of anaesthetized mechanically ventilated rabbits: (A) one with intact NO production, (B) one with intact NO production and where end-tidal CO(2) was controlled, and (C) one with endogenous NO synthesis blockade (L: -NAME, 30 mg kg(-1)). Air infusions resulted in increased FeNO of the control group from 20 (4) [mean (SD)] ppb to a peak value of 39 (4) ppb within 5 min (P < 0.05), and FeNO was still significantly elevated [27 (2) ppb] after 20 min (P < 0.05). Parallel to the NO increase there were significant decreases in end-tidal CO(2 )(ETCO(2)) and mean arterial pressure and an increase in insufflation pressure. In group B, when CO(2) was supplemented after air infusion, NO was suppressed (P = 0.033), but was still significantly elevated compared with pre-infusion control (P < 0.05). In group C, all animals died within 40 min of air infusion whereas all animals in the other groups were still alive at this time point. We conclude that venous air embolization increases FeNO, and that a part of this effect is due to the concomitant decrease in ETCO(2). Furthermore, an intact NO production may be critical for the tolerance to VGE. Finally, FeNO might have a potential in the diagnosis and monitoring of pulmonary gas embolism.

Embolismo gaseoso cerebral por accidente de buceo / Cerebral gas embolism as a result of diving accident

La patología relacionada con los accidentes de buceo es quizás poco conocida por su baja prevalencia. Se clasifica en no disbárica o disbárica, en función de su relación con cambios de presión. Presentamos el caso de un buceador que, después de realizar una inmersión de 30 minutos a 22 metros de profundidad, presentó bradipsiquia y afasia transitoria. En la tomografía axial computarizada craneal se objetivó un infarto silviano izquierdo. Se realizó tratamiento en cámara hiperbárica con buena evolución clínica. En relación con el caso, revisamos las distintas formas de presentación de los accidentes disbáricos, así como la utilidad de la cámara hiperbárica en el tratamiento

Clinical alterations related to diving accidents are little known perhaps because of its low prevalence. They can be classified as dysbarism-related and non-dysbarism-related according to its relation with pressure changes. We present the case of a diver that showed bradypsychia and transitory aphasia after carrying out an immersion of 30 minutes in duration and 22 meters deep. A left sylvian cerebral infarct was demostrated in cranial computerized axial tomography. Treatment was carried out in a hyperbaric chamber with good clinical evolution. We review with regard to this case the different forms of clinical presentation of dysbarism-related accidents, as well as the usefulness of the hyperbaric chamber in their treatment

Embolias gaseosas y terapia por oxigenación hiperbárica durante la gestación / Uterine rupture secondary to dinoprostone in association with epidural analgesia

Aportamos el caso de una mujer embarazada que presentó una embolia paradójica gaseosa subsiguiente a la desconexión del catéter de una vía venosa central. La instalación secundaria de una hemiplejía derecha asociada con un síndrome confusional justificó el tratamiento de urgencia por oxigenoterapia hiperbárica, lo que permitió la remisión completa del cuadro neurológico inicial. La presentación de este caso clínico pone en primer plano la discusión de los riesgos de embolia gaseosa durante el embarazo y el posparto, las indicaciones y los efectos de la oxigenoterapia hiperbárica sobre el feto (AU)

Gas embolism: pathophysiology and treatment.

Based on a literature search, an overview is presented of the pathophysiology of venous and arterial gas embolism in the experimental and clinical environment, as well as the relevance and aims of diagnostics and treatment of gas embolism. The review starts with a few historical observations and then addresses venous air embolism by discussing pulmonary vascular filtration, entrapment, and the clinical occurrence of venous air emboli. The section on arterial gas embolism deals with the main mechanisms involved, coronary and cerebral air embolism (CAE), and the effects of bubbles on the blood-brain barrier. The diagnosis of CAE uses various techniques including ultrasound, perioperative monitoring, computed tomography, brain magnetic resonance imaging and other modalities. The section on therapy starts by addressing the primary treatment goals and the roles of adequate oxygenation and ventilation. Then the rationale for hyperbaric oxygen as a therapy for CAE based on its physiological mode of action is discussed, as well as some aspects of adjuvant drug therapy. A few animal studies are presented, which emphasize the importance of the timing of therapy, and the outcome of patients with air embolism (including clinical patients, divers and submariners) is described.

Embolic inner ear decompression illness: correlation with a right-to-left shunt.

OBJECTIVES/HYPOTHESIS: Inner ear decompression illness is thought to be a rare phenomenon in recreational divers, isolated signs and symptoms of inner ear dysfunction usually being attributed to inner ear barotrauma. STUDY DESIGN: We present 11 cases of inner ear dysfunction in nine divers with inner ear decompression illness. RESULTS: All nine divers had significant right-to-left shunt as diagnosed by transcranial Doppler sonography. CONCLUSIONS: The authors thought that mechanism of causation in these cases may have been intravascular bubble emboli and that inner ear decompression illness may be more common among recreational divers than currently recognized. Failure to treat inner ear decompression illness with recompression therapy can result in permanent disability. Because the differential diagnosis between inner ear barotrauma and inner ear decompression illness can be impossible, the authors suggested that divers who present with inner ear symptoms following a dive should have recompression immediately after having undergone bilateral paracentesis.

Patent foramen ovale and paradoxical systemic embolism: a bibliographic review.

A patent foramen ovale (PFO) has been reported to be an important risk factor for cardioembolic cerebrovascular accidents through paradoxical systemic embolization, and it provides one potential mechanism for the paradoxical systemic embolization of venous gas bubbles produced after altitude or hyperbaric decompressions. Here, we present in a single document a summary of the original findings and views from authors in this field. It is a comprehensive review of 145 peer-reviewed journal articles related to PFO that is intended to encourage reflection on PFO detection methods and on the possible association between PFO and stroke. There is a heightened debate on whether aviators, astronauts, and scuba divers should go through screening for PFO. Because it is a source of an important controversy, we prefer to present the findings in the format of a neutral bibliographic review independent of our own opinions. Each cited peer-reviewed article includes a short summary in which we attempt to present potential parallels with the pathophysiology of decompression bubbles. Two types of articles are summarized, as follows. First, we report the original clinical and physiological findings which focus on PFO. The consistent reporting sequence begins by describing the method of detection of PFO and goal of the study, followed by bulleted results, and finally the discussion and conclusion. Second, we summarize from review papers the issues related only to PFO. At the end of each section, an abstract with concluding remarks based on the cited articles provides guidelines.

[Venous air embolism]. / Venine oro embolija.

Venous air embolism is the entry of air into the venous system as a consequence of trauma or iatrogenic complications (especially central venous cannulation or pressurized intravenous infusion systems). It also can occur following the surgical procedures. Venous air embolism results in right ventricular dysfunction and pulmonary injury. In this review article various causes, frequency, pathophysiology, clinical features, diagnosis, treatment, outcome and prevention of venous air embolism are discussed.