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Background: Our goal was to create a clinically relevant large animal model of pulmonary hypertension to serve as a platform allowing preclinical risk/benefit assessment of innovative therapies including artificial lung prototypes., Methods: Small amounts of filtered air were continuously infused into the pulmonary circulation of sheep (n = 4) for 8 wk. Hemodynamics and blood gases were measured daily. After termination of air embolization, the sheep were observed for 1 additional wk to assess the constancy of the pulmonary artery pressure changes. At the end of wk 9, all sheep were sacrificed and necropsy was performed., Results: All animals survived the study and developed pulmonary hypertension by wk 5. Mean pulmonary artery pressures were elevated from 14 ± 1 at baseline to 35 ± 1 mmHg at wk 8 (P < 0.01) and remained unchanged throughout wk 9. A similar increase in pulmonary vascular resistance was observed. Systemic arterial pressure and PaO(2) dropped slightly compared with baselines but remained in safe ranges. Histologic evidence of severe pulmonary arterial remodeling and significant right ventricle hypertrophy was observed., Conclusions: We conclude that our 8-wk model of continuous air embolization produces reliable, chronic pulmonary hypertension in sheep with sustained hemodynamic changes, significant pulmonary vascular remodeling, and right ventricle hypertrophy., (Copyright © 2011. Published by Elsevier Inc.)

Objective: To describe for the first time, to our knowledge, a case of recurrent in-flight-dependent seizures related to commercial airline flight in which the patient experienced a fatal air embolism secondary to a giant bronchogenic cyst., Design: Case report., Setting: University hospital., Patient: A female airline passenger presented with a seizure, then unconsciousness and death. The patient had experienced 2 previous episodes of in-flight seizures without any sequelae., Results: The patient had an air embolism proved by findings on cranial computed tomography (CT) and a CT perfusion study. The embolism was secondary to a giant bronchogenic cyst that was evident on chest CT. The patient was examined after the previous episodes of in-flight seizures, but no chest radiography had been performed., Conclusions: We propose minor air embolism as a cause of in-flight seizures. This type of seizure can signify the existence of a giant bronchogenic cyst. We believe that obtaining a chest radiograph can be useful in patients with a history of in-flight seizures to rule out the presence of a bronchogenic cyst and to prevent a possibly fatal air embolism.

Background: Transcervical resection of myomas (TCR-M) is considered a safe hysteroscopic procedure if intravasation is limited. Complications may occur if gas formation during myoma resection leads to gaseous embolism. However, the incidence of emboli during transcervical myoma resection is unknown. Therefore in this study the occurrence of physiological changes that indicate the formation of emboli was retrospectively determined in patients undergoing hysteroscopic myoma resection. In addition, these changes were related to the amount of fluid intravasation., Methods: The anesthesia records and operation files of 234 patients were screened for physiological changes that indicate embolism, as measured with standard intraoperative monitoring. These patients underwent surgery for intrauterine myomas with either a monopolar resectoscope with electrolyte-free distension fluid containing 3% sorbitol (limited to 1500-mL intravasation) or a bipolar resectoscope with normal saline solution (limited to 2500-mL intravasation). The patients were grouped according to the amount of fluid intravasation during the operation: Group 1: 500 mL or less, group 2: 500-1000 mL, group 3: 1000-1500 mL, and group 4: 1500-2500 mL., Results: Physiological changes that could be attributed to gaseous embolism were observed in 33% to 43% of patients with 1000 to 2500 mL fluid intravasation during transcervical myoma resection. Nearly half of those patients had cardiovascular disturbances that indicated the formation of emboli., Conclusion: During transcervical resection of myomas, physiological changes that could be attributed to gaseous embolism frequently occurred. Therefore cardiovascular disturbances that indicate gaseous embolism during transcervical resection of myomas may occur despite the limitation of intravasation according to current view., (Copyright © 2011 AAGL. Published by Elsevier Inc. All rights reserved.)

We present the case of an 8-month-old infant with a small bowel obstruction secondary to an ileocolic intussusception without a pathologic lead point. During pneumatic reduction, the patient went into cardiopulmonary arrest, at which point portal venous gas (PVG) was visualized on radiography. Here we present-to our knowledge-the first reported case of PVG secondary to pneumatic reduction of an intussusception along with a review of the literature regarding known complications of pneumatic reduction and the etiologies of PVG., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Rationale and Objectives: To determine the potential of multidetector computed tomography (MDCT) in assessing, at 72 hours, the effects of distal coronary microembolization on myocardial structure and function., Materials and Methods: Microembolic material (total volume=16 mm(3) of 40-120 μm diameter) was selectively delivered in the left anterior descending coronary artery under x-ray fluoroscopy (n = 6 pigs). After 72 hours, 64-slice MDCT was used to assess LV function, perfusion, and viability. For comparison between the measurements at 80 kV, 120 kV, and postmortem we used Bland-Altman and Pearson correlation. Histochemical and histopathological staining was used for quantitative and qualitative characterization of microinfarct., Results: Cine MDCT showed the deleterious effects of microembolization on systolic wall thickening, LV volumes, and ejection fraction. Perfusion parameters, such as max upslope, peak attenuation, and time to peak, differed between microinfarct territory and remote myocardium. Inconsistency in visualizing microinfarct was observed using tube voltages of 80 kV and 120 kV. The extent of heterogeneous microinfarct was 4.5 ± 1.0 % of LV mass at 80 kV, 6.1 ± 0.9% LV at 120 kV, and 5.9 ± 1.1% LV on postmortem. There was significant difference in the extent of microinfarct measured on 80 kV MDCT compared with 120 kV and postmortem. Microscopic examination revealed the random distribution of obstructed microvessels surrounded by myocardial necrosis and inflammatory cells in all animals., Conclusion: Both visible and nonvisible microinfarct cause perfusion deficit and LV dysfunction. MDCT is sensitive for quantifying early functional changes in LV caused by microembolization. Further improvement in spatial resolution of this technology is needed to improve visualization of microinfarct., (Copyright © 2011 AUR. Published by Elsevier Inc. All rights reserved.)

Air embolism in the arterial system is a very rare but potentially fatal complication of percutaneous transthoracic needle biopsy or marking. We report a case of a patient with interstitial pneumonia associated with Sjögren syndrome, who presented with systemic arterial air embolism as a complication of computed tomography-guided marking of the lung. The air inflow route was depicted clearly on computed tomography from the peripheral pulmonary vein that crossed the needle pathway to the left atrium.

Cerebral arterial gas embolism is a risk in diving and occurs as a complication in surgery and interventional radiology. Swine models for cerebral arterial gas embolism have been used in the past. However, injection of air into the main artery feeding the pig brain - the ascending pharyngeal artery - might be complicated by the presence of the carotid rete, an arteriolar network at the base of the brain. On the other hand, anastomoses between external and internal carotid territories are present in the pig. In order to determine the most appropriate vessel for air injection, we performed experiments in which air was injected into either the ascending pharyngeal artery or the external carotid artery. We injected 0.25 ml/kg of room air selectively into the ascending pharyngeal artery or the external carotid artery of 35-40 kg Landrace pigs (n=8). We assessed the effect on cerebral metabolism by measuring intracranial pressure, brain oxygen tension and brain glucose and lactate concentrations using cerebral microdialysis. Intracranial pressure and brain oxygen tension changed significantly in both groups, but did not differ between groups. Brain lactate increased significantly more in pigs in which air was injected into the ascending pharyngeal artery. Intracranial pressure, brain oxygen tension and brain lactate correlated after injection of air into the ascending pharyngeal artery, but not after injection into the external carotid artery. Our model is suitable for investigation of cerebral arterial gas embolism. The ascending pharyngeal artery is the most appropriate vessel for air injection., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Interactions of gas embolism bubbles with endothelial cells, as can occur during decompression events or other forms of intravascular gas entry, are poorly characterized. Endothelial cells respond to microbubble contact via mechanotransduction responses that can lead to cell death or aberrant cellular function. Cultured bovine aortic endothelial cells were individually contacted with microbubbles. Cells were loaded with fluorescent dyes indicating calcium- and nitric oxide-signaling and cell viability. A surfactant, Pluronic F-127, and/or albumin were added to the culture media. Control experiments utilized calcium-free media as well as probe-poking in place of microbubble contact. We acquired fluorescence microscopy time-lapse images of cell responses to bubble and probe contact and determined contact effects on cell signaling and cell death. Calcium influx was essential for cell death to occur with bubble contact. Bubble contact stimulated extracellular calcium entry without altering nitric oxide levels unless cell death was provoked. Cell responses were independent of bubble contact duration lasting either one or 30 seconds. Microbubble contact provoked cell death over seven times more frequently than micropipette poking. Albumin and the surfactant each attenuated the calcium response to bubble contact and also reduced the lethality of microbubble contact by 67.4% and 76.0%, respectively, when used alone, and by 91.2% when used together. This suggests that surface interactions between the bubble or probe interface and plasma- and cell surface-borne macromolecules differentially modulate the mechanism of calcium trafficking such that microbubble contact more substantially induces cell death or aberrant cellular function. The surfactant findings provide a cytoprotective approach to mitigate this form of mechanical injury.

A 29-year-old man was shot in the chest twice sustaining extensive contusion of the right lung. He was, however, clinically stable with no major vessel injury or significant blood loss. Unexpected cardiac arrest occurred hours after hospital admission due to left coronary artery air embolism. Lung parenchymal damage from the passage of two projectiles within the chest wall close to the pleural cavity had occurred, with disruption of the capillary-alveolar interface and passage of air into the pulmonary venous circulation. While tangential gunshot wounds to the chest wall may rarely cause air embolism, symptoms are usually immediate. The present case demonstrates, however, that death may occur unexpectedly some time after the initial trauma in an individual who is considered clinically stable.

Venous air embolism activates platelets in vitro and can evoke platelet dysfunction in swine. We tested the hypothesis that venous air embolism during semi-sitting craniotomy induces thrombocytopenia in humans. We analysed the charts of 799 patients who had an elective craniotomy in the semi-sitting position between 1990 and June 2009. Venous air embolism occurred in 52 patients (6.5%) and was associated with a decrease in mean (SD) in platelet count from 270 (75) × 10⁹ l⁻¹ to 194 (62) × 10⁹ l⁻¹ (p < 0.001). In age-matched controls without venous air embolism mean (SD) platelet count did not change (254 (82) × 10⁹ l⁻¹ vs. 250 (97) × 10⁹ l⁻¹ (NS). While mean (SD) haematocrit fell slightly in both groups (venous air embolism: 0.40 (0.05) to 0.32 (0.04), p <0.001; no venous air embolism: 0.41 (0.04) to 0.35 (0.05), p < 0.001), normalising platelet count to haematocrit did not alter the results., (© 2010 The Authors. Anaesthesia © 2010 The Association of Anaesthetists of Great Britain and Ireland.)

We herein report a patient with decompensated cirrhosis secondary to autoimmune hepatitis, who presented with pneumatosis intestinalis (PI) and portal venous gas. Mesenteric ischemia has been recognized as a common and life-threatening cause of PI which portends a grave prognosis. The patient was found to have bacterascites and recovered after appropriate antibiotic therapy. Spontaneous bacterial peritonitis/bacterascites with gas-forming organisms manifesting as PI has not been previously reported.

Objectives: To evaluate technical success rate and clinical outcome of patients with acute embolic superior mesenteric artery (SMA) occlusion who were treated with primary percutaneous revascularization., Methods: At three medical centers the radiological information system databases were used to identify all patients in whom primary percutaneous revascularization for the treatment of acute embolic SMA occlusion was attempted between 2001 and 2010. Percutaneous treatment was performed in 15 patients (median age 80 years, range 49-88 years). These patients represent the study population. Eleven patients reported abdominal pain. Five patients exhibited peritoneal signs. Revascularization was defined as complete technical success if (1) patency of the SMA with residual stenosis of not more than 30% in diameter and (2) sufficient perfusion of the entire bowel were obtained., Results: Complete technical success was achieved in eleven patients. After percutaneous revascularization laparotomy was performed in six patients and in three of them bowel resection was carried out (length of resected segments 20-80 cm). The 30-day mortality was 33% (five of 15 patients). None of the surviving patients exhibited short-bowel syndrome., Conclusions: Primary percutaneous aspiration and thrombolysis constitutes a promising alternative to surgical revascularization in selected patients with acute embolic SMA occlusion.

Adverse events associated with hysteroscopic procedures are in general rare, but, with increasing operative complexity, it is now apparent that they are experienced more often. A spectrum of complications exist ranging from those that relate to generic components of procedures such as patient positioning and anesthesia and analgesia, to a number that are specific to intraluminal endoscopic surgery (perforation and injuries to surrounding structures and blood vessels). The response of premenopausal women to excessive absorption of nonionic fluids deserves special attention. There is also an increasing awareness of uncommon but problematic sequelae related to the use of monopolar uterine resectoscopes that involve thermal injury to the vulva and vagina. The uterus that has previously undergone hysteroscopic surgery can behave in unusual ways, at least in premenopausal women who experience menstruation or who become pregnant. Better understanding of the mechanisms involved in these adverse events, as well as the use or development of several devices, have collectively provided the opportunity to perform hysteroscopic and resectoscopic surgery in a manner that minimizes risk to the patient., (Copyright 2010 Elsevier Inc. All rights reserved.)

Decompression sickness causes injury and death in SCUBA divers when air bubbles obstruct the flow of blood. Platelets aggregate in response to gas and promote inflammation. Inflammation in decompression sickness may have its origin in the innate immune system's response to pathogens. Bubbles are often found in tissues during gas-forming infections and in infection-prone states. In these diseases, intravascular gas offers a signal of infection to immune cells. Platelet activation by gas may often accompany a beneficial immune response to pathogens. Pathologic bubble-platelet interaction in decompression illness may be an example of gene-environment mismatch., (Published by Elsevier Ltd.)

Background: Chronic haemodialysis (HD) may relieve some medical problems of terminal uraemia, but the life expectancy of patients is still significantly shortened, and there is a greatly increased morbidity. This includes pulmonary morbidity and chronic central nervous system (CNS) abnormalities. Previous studies have shown that a considerable amount of air microbubbles emanate within the blood lines of the dialysis device and pass the air detector without sounding an alarm. The aim of this study was to investigate whether microemboli can pass to the patient and whether they could be detected in the carotid artery., Methods: A total of 54 patients on chronic HD (16 with central dialysis catheter) were investigated with an ultrasound detector (Hatteland, Røyken, Norway) for the presence of microemboli at the arteriovenous (AV) fistula/graft and at the common carotid artery before and during HD. Measurements were taken for 2 and 5 min, respectively. Non-parametric paired statistics were used (Wilcoxon)., Results: The median number (range) and mean +/- SD of microembolic signals detected at the AV access site before commencing dialysis and during HD were 0 (0-3) and 0.2+/- 0.5 versus 4 (0-85) and 13.5 +/- 20 (P = 0.000); at the carotid artery, 1 (0-14) and 1.7 +/- 2.9 versus 2 (0-36) and 3.5 +/- 5.8 (P = 0.008)., Conclusions: The infused and returning fluid from HD devices contains air microbubbles that enter the patient without triggering any alarms. These small emboli pass the lung and may cause ischaemic lesions in organs supported by the arterial circuit, such as the brain.

The maternal respiratory tract undergoes significant anatomic and physiologic changes during pregnancy, which increase maternal susceptibility to respiratory failure. Respiratory failure in pregnancy is relatively rare, but it remains one of the leading conditions requiring intensive care unit admission in pregnancy and carries a high risk of maternal and fetal morbidity and mortality. Acute respiratory failure can result from a variety of conditions, most of which are not pulmonary in origin. Early diagnosis of underlying disease is critical, as it will guide the management approach. Treatment goals during respiratory failure in the pregnant woman are similar to those outside of pregnancy-to maintain adequate ventilation and to provide hemodynamic and nutritional support. Additionally, the obstetrician will need to monitor fetal status and help to determine the best timing for delivery.

Neurologic and neurocognitive complications after cardiac surgery have been reported repeatedly. To better understand its etiology and design protective strategies, small animal models have been developed. This study describes the development of a survival rat cardiopulmonary bypass (CPB) model, along with the introduction of an appropriately sized oxygenator. This model led the way for even more complicated models with CPB, facilitating full cardiac arrest with anterograde cardioplegia administration, air embolization, and deep hypothermic circulatory arrest. In addition, the results of several of those rat CPB studies are summarized and their preclinical relevance is pointed out.

Background: Mild hypothermia has become an important treatment for ischemic brain injury. However, the role of mild hypothermia in air embolism-induced lung injury has not been explored. In this study, we investigated whether treatment with mild hypothermia before and synchronous with air infusion can attenuate acute lung injury induced by air embolism., Methods: In this rat model study (Sprague-Dawley rats), pulmonary air embolism was induced by venous infusion of air at a rate of 25 microL/min for 40 minutes. Control animals received no air infusion. The rats were randomly assigned to 2 control groups of normothermia (37 degrees C) and mild hypothermia (34 degrees C) and 3 air embolism groups of mild hypothermia induced before air infusion, normothermia with air infusion, and mild hypothermia induced synchronous with air infusion. At the end of the experiment, the variables of lung injury were assessed., Results: Air infusion elicited a significant increase in lung wet/dry weight ratio and protein, lactate dehydrogenase, and tumor necrosis factor-alpha concentration of the bronchoalveolar lavage fluid. Myeloperoxidase activity, neutrophil infiltration, and interstitial edema in lung tissue were also significantly increased. In addition, nuclear factor-kappaB activity was significantly increased in the lungs. Treatment with mild hypothermia before air infusion reduced increases in these variables, whereas mild hypothermia synchronous with air infusion had no significant effect on them., Conclusions: Our study suggests that mild hypothermia before air infusion decreases air embolism-induced acute lung injury. The protective mechanism seems to be the inhibition of inflammation.

Iatrogenic gas embolism is a rare but serious problem that has been documented in almost all medical specialties including gynecology. We present a 49-year-old woman undergoing operative hysteroscopy and myomectomy, who sustained sudden hypotension and decrease in the end-tidal carbon dioxid levels during the procedure. Systemic gas embolism was confirmed by echocardiographic evidence of bubbles in both right and left cardiac cavities and a rise of troponin. Hyperbaric oxygen was rapidly administered in addition to maintenance of vital functions and anti-thrombotic prevention with calciparin. A right hemiparesis was apparent after recovery from general anesthesia. Brain-computed tomography and magnetic resonnance imaging, performed on Days 3 and 2 respectively, showed a left fronto-parietal hematoma surrounded by edema. Having ruled out risk factors for a primary ischemic or hemorrhagic stroke, we concluded that hemorragic transformation of the ischemic cerebral lesion caused by gas embolism was responsible for the observed intraparenchymal hematoma. As far as we know, this is the first report relating cerebral gas embolism with an intracerebral hemorrhage. It provides an argument against anticoagulant therapy during the early stages of gas embolism care.

A 72 year-old woman with cholangiocarcinoma presented for endoscopic retrograde cholangio pancreatography (ERCP) for diagnostic intraductal endoscopy under GETA. During the technically difficult procedure the patient became suddenly hypoxic, hypotensive, bradycardic, and progressed to PEA code (ETCO2 5 mmHg). ACLS was initiated. Transesophageal echo demonstrated massive right heart air accumulation; abdominal X-Ray showed air filled bile ducts. Central access was obtained, a pulmonary artery catheter floated, and 30 ml of air aspirated from the RV. Within 5 minutes pulses returned; the patient was transferred to the ICU. MRI revealed two watershed infarcts in the right frontal lobe. The patient fully recovered and returned a month later for an uneventful ERCP.

We report a rare case of a massive fatal embolism that occurred in the middle of endoscopic retrograde cholangiopancreatography (ERCP) and retrospectively examine the significant causes of the event. The patient was a 50-year old female with an uncertain history of previous abdominal surgery for multiple biliary stones 20 years prior. The patient presented with acute right upper quadrant pain. An abdominal computed tomographic (CT) scan revealed the presence of multiple stones in the common bile duct (CBD) and intra-hepatic duct (IHD) with biliary obstruction, multifocal liver abscesses, and air-biliarygram. Emergency ERCP showed a wide and straight opening of choledochoduodenostomy, which may have been created during a previous surgery, and multiple filling defects in the CBD. With the use of a forward endoscope, mud stones were extracted through the opening of the choledochoduodenostomy. Cardiac arrest suddenly developed during the procedure, and despite immediate resuscitation, the patient died due to a massive systemic air embolism. We reviewed previously reported fatal cases and accessed factors facilitating air embolisms in this case.

Central venous catheters are widely used in clinical practice. Air embolism is a rare, but potentially life threatening complication of central venous catheterisation. We describe a case of collapse and transient hemiplegia after removal of central venous catheter. This was accidentally performed with the patient in upright position. A CT scan of the brain demonstrated air in the sinus cavernosus bilaterally and at the posterior wall of the foramen magnum.

Venous thromboembolism (VTE) can be considered a multifactorial disorder involving a variety of inherited and acquired prothrombotic conditions and events. Although greater emphasis has classically been given to traditional thrombophilic risk factors, there is increasing recognition of less typical precipitating conditions and events. Indeed, the list of plausible but unusual triggers of thrombosis includes sneezing and coughing attacks, eating, migraine, sexual intercourse, strenuous physical exercise, drug abuse, and defecation. Although it is difficult to assert conclusively the true contribution of such events to the etiology of acute episodes of venous thrombosis, it seems reasonable to conclude that the concomitant presence of such trivial elements with one or more additional risk factors for VTE might precipitate an acute thrombotic episode., ((c) Thieme Medical Publishers.)

Pneumocephalus in the absence of a recent intracranial or intrathecal procedure is a significant radiographic finding and may be clinically relevant. Pneumocephalus secondary to intravenous catheterization may be a more common finding than previously expected. Although pneumocephalus is often associated with pathological conditions, recognition of a characteristic pattern of intravenous pneumocephalus in the presence of intravenous catheterization may aid the clinician in determining a patient's underlying condition. This unexpected radiographic finding should not necessarily be cause for alarm, and there is no evidence that intravenous pneumocephalus alone is harmful. We present a patient with intravenous pneumocephalus and a review of the literature.

We describe a case of intraoperative neonatal cardiac arrest during attempted laparoscopic surgery. Circulatory collapse occurred before peritoneal insufflation, initially obscuring the diagnosis. Emergent transthoracic echocardiography during resuscitation demonstrated intracardiac gas bubbles consistent with venous gas embolism. The site of entrainment was probably a bleeding umbilical vein transected by the umbilical trocar. Greater awareness of this complication in neonates will facilitate early diagnosis and encourage preventive measures, such as the avoidance of umbilical vessels, use of an open instead of closed access technique, and ligation of bleeding vessels after peritoneal access.

A young man was admitted for a polytraumatism associating head trauma and blunt abdominal trauma with hepatic injury. He was managed with a damage control surgery with a perihepatic packing. During the second look surgery, he developed a paradoxal gazous embolism by air aspiration in the sus-hepatic vein. This has never been described before in such traumatism. The patient presented a respiratory distress, a circulatory shock due to right infarction and an intracranial hypertension with bilateral mydriasis. He was immediately treated by hyperbaric oxygenotherapy. The evolution was good and he recovered without sequelae.

Background and Purpose: Baicalin has been reported to have anti-inflammatory effects and protect against various tissue injuries. However, the effect of baicalin on air embolism-induced acute lung injury has not been tested yet., Experimental Approach: Acute lung injury was induced by infusion of air at a rate of 0.25 mL.min(-1) for 1 min into the pulmonary artery of rat isolated lungs. At the end of the experiment, samples were collected for assessment of lung injury, biochemical analysis and histology. Different doses of baicalin (1, 2 and 4 mg.kg(-1)) were given into the perfusate before air infusion., Key Results: Air embolism elicited a significant increase in microvascular permeability (K(f)), lung weight gain, wet/dry weight ratio, pulmonary artery pressure and protein concentration in the bronchoalveolar lavage fluid. Levels of the cytokines, tumour necrosis factor alpha and cytokine-induced neutrophil chemoattractant-1 in perfusate, and malondialdehyde levels and myeloperoxidase activities in lung tissue were also significantly increased. In addition, histological examination showed increased neutrophil infiltration in lung tissues. Furthermore, nuclear factor-kappaB activity and degradation of IkappaB-alpha were significantly increased in lungs. Pretreatment of the lungs with baicalin (4 mg.kg(-1)) showed a statistically significant difference in all of the assessed parameters, except for alteration in the pulmonary artery pressure., Conclusions and Implications: Our study suggests that baicalin attenuated air embolism-induced acute lung injury and may be considered a useful adjunct drug therapy in this clinical condition.

We presented the case of a neonate with portal venous gas and pulmonary gas embolism. The patient presented with severe respiratory distress and abdominal distension 12 hours after birth. An ultrasound revealed intravascular microbubbles moving into a pulmonary artery that were traveling from the portal venous system through a ductus venosus. Additional clinical observations were hypotension and a sudden decrease in end-tidal carbon dioxide with a markedly discrepant high Pco(2), indicating a massive pulmonary gas embolism. Operative findings revealed congenital ileal atresia and meconium peritonitis with abscess. Gas-forming Escherichia coli was recovered from the abscess contents. The patient had respiratory distress, shock, disseminated intravascular coagulation, and intractable diarrhea but eventually recovered and was discharged on the 131st postoperative day.

Background: Focal neurological deficits following cardiopulmonary bypass surgery are usually thought to be the result of embolic stroke. Computed tomography (CT) is sometimes negative although severe deficits persist., Objectives: To describe a syndrome consisting of reduced postoperative vigilance, frequent epileptic seizures and focal neurological deficits in the presence of an apparently normal CT scan and often isolated cortical infarction on magnetic resonance imaging (MRI)., Methods: We retrospectively collected data on all patients fulfilling the above-mentioned criteria, seen for neurological examination by the consultant between 2002 and 2006 in our heart center., Results: We found 39 patients, nearly all of whom had cortical hyperintense lesions on diffusion-weighted MRI in the right hemisphere with corresponding left-sided hemiparesis. Early seizures occurred in 31 patients. Clinical outcome was heterogeneous., Conclusions: Predominance of right hemisphere involvement and lesion pattern in MRI make air embolism the most probable cause for this postoperative syndrome.

Air embolism in the coronary arteries is a known complication of coronary angiography. Diving is a non-iatrogenic cause of arterial air embolism, commonly presenting with neurological and musculoskeletal symptoms. This is the first known case of coronary air embolism confirmed on coronary angiography in a diver presenting with pulmonary edema secondary to acute coronary syndrome. The possible mechanisms of coronary air embolism during a dive are reviewed in this article.

Objective: Paradoxical gas embolism through right-to-left (R/L) shunts is considered as a potential cause of certain types of decompression sickness., Aim: To assess whether 4 months of repetitive diving and strenuous exercises would lead to an increased prevalence of R/L shunting in a group of military divers., Methods: Using a standardised contrast-enhanced transcranial Doppler technique, 17 divers were re-examined for the presence of a R/L shunt 4 months after their initial examinations. R/L shunts were classified as type I if observed only after a straining manoeuvre, and type II if present at rest., Results: Initial prevalence of R/L shunt was 41%: six type I shunts and one type II. At the second examination, prevalence was 47%, with the appearance of one type I shunt that was not previously present. We found no significant increase in the prevalence and size of R/L shunts., Conclusion: It is speculated that diving-related phenomena, such as variations in right atrial pressures during the end stages of or events immediately after a dive could generate an R/L shunt. However, extreme conditions of repetitive diving and strenuous exercises do not cause permanent modification in R/L permeability over a period of 4 months.