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Gas embolism
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Background:
Air embolism is a rare, but potentially catastrophic complication of endoscopic procedures. We herein evaluated the overall incidence of air embolism after endoscopy. We also measured mortality outcomes after air embolism.
Methods:
Patients who underwent endoscopy as an index procedure during hospitalization were selected from the National Inpatient Sample from 1998-2013. The primary outcome of interest was the incidence of air embolism after endoscopy. All-cause mortality after endoscopy was measured as a secondary outcome and the Charlson Comorbidity Index was calculated. Binary logistic regression was used to explore the effect of air embolism on inpatient mortality, using P<0.05 as level of significance.
Results:
A total of 2,245,291 patients met the inclusion criteria. Mean age at the time of procedure was 62.5 years. Esophagogastroduodenoscopy (EGD) was the most common endoscopic procedure, accounting for 80% of endoscopic procedures. Air embolism occurred in 13 cases, giving a rate of 0.57 per 100,000 endoscopic procedures. Air embolism was most common after endoscopic retrograde cholangiopancreatography (ERCP), occurring in 3.32 per 100,000 procedures, compared with 0.44 and 0.38 per 100,000 procedures for EGD and colonoscopy, respectively. The case fatality rate for post endoscopic air embolism was 15.4%. After adjusting for covariates, air embolism after endoscopy was independently associated with higher odds of inpatient mortality: odds ratio 10.35, 95% confidence interval 1.21-88.03 (P<0.03).
Conclusions:
Air embolism is most common after ERCP. It is frequently associated with disorders involving a breach to the gastrointestinal mucosa or vasculature. Though rare, it is an independent predictor of inpatient mortality.
Air embolism is an uncommon, but potentially life-threatening event for which prompt diagnosis and management can result in significantly improved patient outcomes. Most air emboli are iatrogenic. Arterial air emboli may occur as a complication from lung biopsy, arterial catheterization or cardiopulmonary bypass. Immediate management includes placing the patient on high-flow oxygen and in the right lateral decubitus position. Venous air emboli may occur during pressurized venous infusions, or catheter manipulation. Immediate management includes placement of the patient on high-flow oxygen and in the left lateral decubitus and/or Trendelenburg position. Hyperbaric oxygen therapy is the definitive treatment which may decrease the size of air emboli by facilitating gas reabsorption, while also improving tissue oxygenation and reducing ischemic reperfusion injury.
A 51-year-old man was admitted to have a nodule evaluated using chest computed tomography (CT). Shortly after curetting and transbronchial biopsies via bronchoscopy, hypotension, bradycardia, unconsciousness, and left hemiplegia appeared and resolved within one hour. Head CT showed cerebral air embolism. The following day, lower left quadrant pain developed. Pneumatosis intestinalis on abdominal CT and elevation of creatine kinase and troponin T levels indicated air embolism in the mesenteric and coronary arteries. Some reports have documented cerebral air embolism alone after bronchoscopy; however, we should consider systemic air embolism, even when encountering a patient without specific symptoms related to any organ.
The anesthesiologist must be aware of the causes, diagnosis and treatment of venous air embolism and adopt the practice patterns to prevent its occurrence. Although venous air embolism is a known complication of cesarean section, we describe an unusual inattention that causes iatrogenic near fatal venous air embolism during a cesarean section under spinal anesthesia. One of the reasons for using self-collapsible intravenous (IV) infusion bags instead of conventional glass or plastic bottles is to take precaution against air embolism. We also demonstrated the risk of air embolism for two kinds of plastic collapsible intravenous fl uid bags: polyvinyl chloride (PVC) and polypropylene-based. Fluid bags without self-sealing outlets pose a risk for air embolism if the closed system is broken down, while the fl exibility of the bag limits the amount of air entry. PVC-based bags, which have more fl exibility, have signifi cantly less risk of air entry when IV administration set is disconnected from the outlet. Using a pressure bag for rapid infusion can be dangerous without checking and emptying all air from the IV bag.
Gastrointestinal endoscopy has become an important modality for the diagnosis and treatment of various gastrointestinal disorders. One of its major advantages is that it is minimally invasive and has an excellent safety record. Nevertheless, some complications do occur, and endoscopists are well aware and prepared to deal with the commonly recognized ones including bleeding, perforation, infection, and adverse effects from the sedative medications. Air embolism is a very rare endoscopic complication but possesses the potential to be severe and fatal. It can present with cardiopulmonary instability and neurologic symptoms. The diagnosis may be difficult because of its clinical presentation, which can overlap with sedation-related cardiopulmonary problems or neurologic symptoms possibly attributed to an ischemic or hemorrhagic central nervous system event. Increased awareness is essential for prompt recognition of the air embolism, which can allow potentially life-saving therapy to be provided. Therefore, we wanted to review the risk factors, the clinical presentation, and the therapy of an air embolism from the perspective of the practicing endoscopist.
Gas microembolism remains a serious risk associated with surgical procedures and decompression. Despite this, the signaling consequences of air bubbles in the vasculature are poorly understood and there is a lack of pharmacological therapies available. Here, we investigate the mitochondrial consequences of air bubble contact with endothelial cells.
Human umbilical vein endothelial cells were loaded with an intracellular calcium indicator (Fluo-4) and either a mitochondrial calcium indicator (X-Rhod-1) or mitochondrial membrane potential indicator (TMRM). Contact with 50-150 µm air bubbles induced concurrent rises in intracellular and mitochondrial calcium, followed by a loss of mitochondrial membrane potential. Pre-treating cells with 1 µmol/L ruthenium red, a TRPV family calcium channel blocker, did not protect cells from the mitochondrial depolarization, despite blocking the intracellular calcium response. Mitigating the interactions between the air-liquid interface and the endothelial surface layer with 5% BSA or 0.1% Pluronic F-127 prevented the loss of mitochondrial membrane potential. Finally, inhibiting protein kinase C-α (PKCα), with 5 µmol/L Gö6976, protected cells from mitochondrial depolarization, but did not affect the intracellular calcium response.
Our results indicate that air bubble contact with endothelial cells activates a novel, calcium-independent, PKCα-dependent signaling pathway, which results in mitochondrial depolarization. As a result, mitochondrial dysfunction is likely to be a key contributor to the pathophysiology of gas embolism injury. Further, this connection between the endothelial surface layer and endothelial mitochondria may also play an important role in vascular homeostasis and disease.
Clinically significant carbon dioxide embolism is a rare but potentially fatal complication of anesthesia administered during laparoscopic surgery. Its most common cause is inadvertent injection of carbon dioxide into a large vein, artery or solid organ. This error usually occurs during or shortly after insufflation of carbon dioxide into the body cavity, but may result from direct intravascular insufflation of carbon dioxide during surgery. Clinical presentation of carbon dioxide embolism ranges from asymptomatic to neurologic injury, cardiovascular collapse or even death, which is dependent on the rate and volume of carbon dioxide entrapment and the patient's condition. We reviewed extensive literature regarding carbon dioxide embolism in detail and set out to describe the complication from background to treatment. We hope that the present work will improve our understanding of carbon dioxide embolism during laparoscopic surgery.
Computed tomography-guided transthoracic lung biopsy is a common clinical procedure for the diagnosis of a broad range of pulmonary pathological conditions. Mild self-limiting pneumothorax and haemoptysis are common complications of this procedure. Air embolism is a potentially life-threatening but extremely rare complication. We report a case of an air embolism in the left ventricle of the heart that developed after a computed tomography-guided percutaneous needle biopsy of the lung. The patient did not exhibit cardiac or cerebral symptoms after conservative treatment. The patient underwent a successful left thoracotomy with a lobectomy of the left lower lobe of the lung 5 days after the biopsy and recovered uneventfully.
Significant venous air embolism may develop acutely during the perioperative period due to a number of causes such as during head and neck surgery, spinal surgery, improper central venous and haemodialysis catheter handling, etc. The current trend of using self collapsible intravenous (IV) infusion bags instead of the conventional glass or plastic bottles has several advantages, one of thaem being protection against air embolism. We present a 56-year-old man undergoing kidney transplantation, who developed a near fatal venous air embolism during volume resuscitation with normal saline in collapsible IV bags used with rapid infuser system. To our knowledge, this problem with collapsible infusion bags has not been reported earlier.
This study was designed to determine the conditions that promote carbon dioxide embolism after venous injury during laparoscopy
in pigs. Injury to an iliac vein was filmed during laparoscopy in the presence of a pneumoperitoneum created at increasing
pressures from 0 to 30 mm Hg in 5-mm Hg increments. At intraperitoneal pressures less than 20 mm Hg, there was a parallel
increase in femoral venous pressures, resulting in haemorrhage, with persistent blood flow to the inferior vena cava. At intraperitoneal
pressures of 20-30 mm Hg, there was collapse of the femoral vein, occurring earlier in the presence of hypovolaemia. Between
these two states (haemorrhage and collapse), there was a point of equilibrium which allowed retrograde venous penetration
of carbon dioxide bubbles. During release of the pneumoperitoneum, these bubbles were exteriorized through the area of the
injury, but some passed into the inferior vena cava where their presence was detected by an oesophageal Doppler probe.
The pathophysiology of arterial air embolism inducing brain injuries remains unclear. Previous experiments demonstrated the usefulness of computed tomography (CT) in the detection of air emboli in canine brain. This canine study investigates CT's ability to detect small air bubbles and to determine the kinetics of air elimination from cerebral arteries and it's relationship with clinical, electroencephalographic (EEG), and histological manifestations. CT detects small air embolism, and intracerebral air volume strongly correlates with injected air dose (r2 = 0.86, p = 2 × 10 3) Air clearance time significantly depends on intracerebral air volume (r2 = 0.86, p = 0 04) and on the number of bubbles (r2 = 0.71, p = 0 03), whereas half–life of air elimination does not. No relationship was found between injected air dose, air clearance time, intracerebral volume of air, and clinical, EEG, and histological findings. The data indicate that CT accurately detects small air bubbles in the early course of cerebral air embolism, that air elimination from cerebral arteries follows a first–order compartment model, and that early CT findings do not correlate with clinical, EEG, and histological manifestations.
: Venous air embolism (VAE) is a potentially life-threatening event that is most commonly associated with certain surgical procedures, although this theoretical complication of pressurized rapid infusion of intravenous (IV) fluids has been described. This series of cases describes 4 athletes who presented with continuous coughing and other chest complaints after peripheral IV infusion of normal saline through manual pressurized infusion. Symptoms resolved within 20 minutes, and these incidences did not interfere with resuming athletic competition with no recurrence of symptoms or complications. These cases are most consistent with varying degrees of VAE and reveal the risk of VAE associated with pressurized peripheral IV fluid administration along with the unique clinical presentation of more modest forms of VAE in an awake patient. Becoming more knowledgeable about IV infusion technique and understanding potential pitfalls can be helpful in reducing future incidences of VAE.
Pressure infusion devices are used in clinical practice to apply large volumes of fluid over a short period of time. Although air infusion is a major complication, they have limited capability to detect and remove air during pressure infusion. In this investigation, we tested the air elimination capabilities of the Fluido® (The Surgical Company), Level 1® (Level 1 Technologies Inc.) and Ranger® (Augustine Medical GmbH) pressure infusion devices. Measurements were undertaken with a crystalloid solution during an infusion flow of 100, 200, 400 and 800 ml.min−1. Four different volumes of air (25, 50, 100 and 200 ml) were injected as boluses in one experimental setting, or infused continuously over the time needed to perfuse 2 l saline in the other setting. The perfusion fluid was collected in an airtight infusion bag and the amount of air obtained in the bag was measured. The delivered air volume was negligible and would not cause any significant air embolism in all experiments. In our experimental setting, we found, during high flow, an increased amount of uneliminated air in all used devices compared with lower perfusion flows. All tested devices had a good air elimination capability. The use of ultrasonic air detection coupled with an automatic shutoff is a significant safety improvement and can reliably prevent accidental air embolism at rapid flows.
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The assumption that the lung is an effective filter for gas bubbles is of importance for certain occupations (e.g., divers, astronauts) as well as in the accomplishment of several medical procedures. The filtering capacity was tested in pigs by use of continuous air infusion into the right ventricle and a transesophageal echocardiographic transducer for detection of air in the left atrium. Twenty pigs, anesthetized with pentobarbital sodium and mechanically ventilated, were divided into groups that received air at infusion rates of 0.05 (group 1a, n = 7), 0.10 (group 2, n = 6), and 0.20 (group 3, n = 5) ml.kg-1.min-1. Two pigs served as controls. The breakthrough incidence was 0, 67, and 100%, respectively. Group 1a received a second infusion of 0.10 ml.kg-1.min-1 (group 1b, n = 7), and spillover of bubbles occurred in only 14% of these pigs. Infusion of gas caused a maximum increase in mean pulmonary arterial pressure (PAP) of 129 +/- 9% to 39.2 +/- 1.3 (SE) mmHg, with no significant difference between the groups. Breakthrough was observed only in animals with a dramatic reduction in mean arterial pressure and a PAP that returned to almost-normal values at spillover time. Our results suggest that the threshold value for breakthrough of air bubbles in pigs is reduced compared with that in dogs. The hemodynamic consequences at a given infusion rate are, however, greatly enhanced.
To assess the safety and efficacy of the maneuver of active lung inflation (ALI) after venous air embolism, measurements were made of pulmonary artery occlusion pressure (PAOP), central venous pressure (CVP), and superior jugular bulb pressure (JbP) as an index of cerebral venous sinus pressure in eight sheep before and after a 2-ml/kg air embolus and before and in the release phase of an ALI to a pressure of 4 kPa (30 mm Hg). (PAOP-CVP) difference decreased significantly after the air embolus with a further decrease after ALI (P less than 0.01). An increase in JbP occurred with ALI only when the CVP was elevated before the injection of air. After air embolism in neurosurgery, ALI may increase the likelihood of paradoxical embolism in patients at risk and may also fail to help in identifying the site of air entry.
Venous air embolism (VAE) is a recognized complication of surgery performed with the patient in the sitting position, but
it occurs also during other operations. We report two cases of VAE, associated with a notable decrease in dynamic lung compliance,
detected by side-stream spirometry. Based on these cases, an experiment with 10 pigs was designed to evaluate the usefulness
of side-stream spirometry in the diagnosis of VAE. Three doses of air (0.5, 1.0 and 2.0 ml kg-1) were injected via the proximal
part of a 5- French gauge pulmonary artery catheter. Only the largest dose was followed by haemodynamic deterioration. Significant
increases in end-tidal oxygen content and decreases in dynamic lung compliance were detected with all doses of air together
with conventional signs of VAE, that is increases in pulmonary artery pressures and arterial carbon dioxide tensions, and
decreases in end-tidal concentration of carbon dioxide. We conclude that continuous monitoring of end-tidal oxygen concentration
and side-stream spirometry offers valuable supplements to other monitoring techniques in the detection of VAE.
Venous gas embolism (VGE) is reported with decompression to a decreased ambient pressure. With severe decompression, or in cases where an intracardiac septal defect (patent foramen ovale) exists, the venous bubbles can become arterialized and cause neurological decompression illness. Incidence rates of patent foramen ovale in the general population range from 25-34% and yet aviators, astronauts, and deepsea divers who have decompression-induced venous bubbles do not demonstrate neurological symptoms at these high rates. This apparent disparity may be attributable to the normal pressure gradient across the atria of the heart that must be reversed for there to be flow patency. We evaluated the effects of: a) venous gas embolism (0.025, 0.05 and 0.15 ml.kg-1.min-1 for 180 min.); b) hyperbaric decompression; and c) hypobaric decompression on the pressure gradient across the left and right atria in anesthetized dogs with intact atrial septa. Left ventricular end-diastolic pressure was used as a measure of left atrial pressure. In a total of 92 experimental evaluations in 22 dogs, there were no reported reversals in the mean pressure gradient across the atria; a total of 3 transient reversals occurred during the peak pressure gradient changes. The reasons that decompression-induced venous bubbles do not consistently cause serious symptoms of decompression illness may be that the amount of venous gas does not always cause sufficient pressure reversal across a patent foramen ovale to cause arterialization of the venous bubbles.
The potential for pulmonary embolization following major venous laceration occurring during laparoscopic surgery has never been evaluated. Five anesthetized dogs were hemodynamically monitored with an arterial line and Swan-Ganz catheter. Observation by transesophageal echocardiography (TEE) allowed comparison with pulmonary artery pressure (PAP) recording. Under pneumoperitoneum, a 1-cm venotomy was performed in the infrarenal vena cava and a total of 11 events were evaluated upon unclamping the venotomy. These results were compared with intravenous (i.v.) bolus injections of 15 cc of CO2 (15 events) and of 100 cc of CO2 (12 events). The animals were maintained euvolemic. In 2 out of the 11 (18%) events which followed unclamping the venotomies, a few CO2 bubbles were seen in the right heart cavities. However, the quantity of gas was much less important than that seen after i.v. injection of 15 cc and 100 cc of CO2. There was no significant elevation of the PAP from pre-event values after venotomy or after i.v. injection of 15 cc of CO2. However, there was a significant difference (P < 0.05) when these results were compared to the PAP values recorded after i.v. injection of 100 cc of CO2. No dog died after these episodes of embolization. Massive i.v. injection of CO2 (> 300 cc) led to appearance of gas bubbles in the left heart cavities and death. This experiment suggests that caution should be exerted when laparoscopic surgery is performed beside large veins. Nevertheless, the observation that no gas embolism occurred in 82% of the cases after unclamping venotomies was unexpected. In contrast, many more gas bubbles were detected in the right heart after i.v. injection of only 15 cc of CO2. TEE is a more sensitive indicator of pulmonary embolization than elevation of PAP.
In this randomized, experimental study in 18 pigs, we have investigated the effects of inspiratory air in oxygen, 100% oxygen
and 50% nitrous oxide in oxygen on the detection and consequences of venous air embolism. Each animal was tested with injections
of 1.0 ml kg-1 and 2.0 ml kg-1 of air. All animals, except one in the nitrous oxide group, survived the air emboli. Systolic
and diastolic arterial pressures decreased significantly in all groups after both injections of air. Pulmonary diastolic pressures
increased most in the nitrous oxide group. End-tidal concentration of carbon dioxide decreased significantly in all groups
after air injections. The difference in concentration of oxygen in the inspiratory and expiratory gas (O2 (I-E)) was lowest
in the air group after both injections of air. On the basis of our studies we suggest that nitrous oxide should not be used
during surgery associated with an increased risk of venous air embolism.
Although the low-flow CO2 insufflation rate used to initiate pneumoperitoneum may reduce the severity of potential venous embolism, its safety is not established.
Anesthetized pigs were ventilated with room air at a fixed minute ventilation. After 1 h of baseline, they were intravenously infused with CO2 at the rate of 0.3, 0.75, or 1.2 ml/kg/min for 2 h (n = 5 for each group), followed by 1 h of recovery.
All animals experienced pulmonary hypertension, depressed stroke volume, hypoxemia, hypercarbia, and acidemia during intravenous CO2 infusion. They had systemic hypertension at the low rate of hypotension at the highest rate of infusion. End-tidal CO2 levels briefly decreased, then increased in all cases. In the highest rate group, three of the five animals (60%) died at 50, 65, and 100 min of infusion. These three animals had severe hypotension and hypoxemia, with visible coronary gas embolism. There was no patent foramen ovale at necropsy in any animals.
The low-flow insufflation rate exceeds the fatal rate of continuous intravenous CO2 infusion. End-tidal CO2 levels were increased in venous CO2 embolism, not decreased as seen in venous air embolism. Severe hypoxemia and hypotension are predictors of potentially fatal cases.
Multifocal cerebrovascular gas embolism occurs frequently during cardiopulmonary bypass and is thought to cause postoperative neurological dysfunction in large numbers of patients. We developed a mathematical model to predict the absorption time of intravascular gas embolism, accounting for the bubble geometry observed in vivo. We modeled bubbles as cylinders with hemispherical end caps and solved the resulting governing gas transport equations numerically. We validated the model using data obtained from video-microscopy measurements of bubbles in the intact cremaster microcirculation of anesthetized male Wistar rats. The theoretical model with the use of in vivo geometry closely predicted actual absorption times for experimental intravascular gas embolisms and was more accurate than a model based on spherical shape. We computed absorption times for cerebrovascular gas embolism assuming a range of bubble geometries, initial volumes, and parameters relevant to brain blood flow. Results of the simulations demonstrated absorption time maxima and minima based on initial geometry, with several configurations taking as much as 50% longer to be absorbed than would a comparable spherical bubble.
We investigated the vagal and mediator mechanisms underlying the tachypnea caused by pulmonary air embolism (PAE) in anesthetized and spontaneously breathing dogs. PAE was induced by infusion of air into the right atrium (0.2 ml. kg(-1). min(-1) for 10 min). The first PAE induction caused an increase in respiratory frequency accompanied by a decrease in tidal volume in each of the 30 animals studied. Subsequently, animals were evenly divided into five groups, and a second PAE induction was repeated after various experimental interventions. The tachypneic response to PAE was not significantly altered by pretreatment with a saline vehicle but was largely attenuated by either perivagal capsaicin treatment (a technique that selectively blocks the conduction of unmyelinated C fibers), pretreatment with ibuprofen (a cyclooxygenase inhibitor), or pretreatment with dimethylthiourea (a hydroxyl radical scavenger). Ultimately, the tachypneic response was nearly abolished by a bilateral cervical vagotomy. These results suggest that 1) lung vagal unmyelinated C-fiber afferents play a predominant role in evoking the reflex tachypneic response to PAE and 2) both cyclooxygenase products and hydroxyl radical are important in eliciting this vagally mediated response.
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.