Iatrogenic air embolism: pathoanatomy, thromboinflammation, endotheliopathy, and therapies

Iatrogenic vascular air embolism is a relatively infrequent event but is associated with significant morbidity and mortality. These emboli can arise in many clinical settings such as neurosurgery, cardiac surgery, and liver transplantation, but more recently, endoscopy, hemodialysis, thoracentesis, tissue biopsy, angiography, and central and peripheral venous access and removal have overtaken surgery and trauma as significant causes of vascular air embolism. The true incidence may be greater since many of these air emboli are asymptomatic and frequently go undiagnosed or unreported. Due to the rarity of vascular air embolism and because of the many manifestations, diagnoses can be difficult and require immediate therapeutic intervention. An iatrogenic air embolism can result in both venous and arterial emboli whose anatomic locations dictate the clinical course. Most clinically significant iatrogenic air emboli are caused by arterial obstruction of small vessels because the pulmonary gas exchange filters the more frequent, smaller volume bubbles that gain access to the venous circulation. However, there is a subset of patients with venous air emboli caused by larger volumes of air who present with more protean manifestations. There have been significant gains in the understanding of the interactions of fluid dynamics, hemostasis, and inflammation caused by air emboli due to in vitro and in vivo studies on flow dynamics of bubbles in small vessels. Intensive research regarding the thromboinflammatory changes at the level of the endothelium has been described recently. The obstruction of vessels by air emboli causes immediate pathoanatomic and immunologic and thromboinflammatory responses at the level of the endothelium. In this review, we describe those immunologic and thromboinflammatory responses at the level of the endothelium as well as evaluate traditional and novel forms of therapy for this rare and often unrecognized clinical condition

Gas embolism during surgery. A complement mediated condition?

Introduction: Venous air embolism (VAE) may arise during surgical procedures. VAE might be complicated with a systemic inflammatory response, disseminated intervascular coagulation, multi-organ failure and cardiovascular collapse. During a short time-span, three patients at our institution developed signs of VAE in conjunction with gynecological surgery. One died, one developed severe cerebral infarctions and one developed myocardial infarction. Previously, air embolisms have been shown to trigger complement C3 and C5 activation in plasma. We have examined in vitro in human whole blood and in vivo in a porcine model, how air triggers inflammation and activation of complement and coagulation and their cross-talk.</p

Gas embolism during surgery. A complement mediated condition?

Introduction: Venous air embolism (VAE) may arise during surgical procedures. VAE might be complicated with a systemic inflammatory response, disseminated intervascular coagulation, multi-organ failure and cardiovascular collapse. During a short time-span, three patients at our institution developed signs of VAE in conjunction with gynecological surgery. One died, one developed severe cerebral infarctions and one developed myocardial infarction. Previously, air embolisms have been shown to trigger complement C3 and C5 activation in plasma. We have examined in vitro in human whole blood and in vivo in a porcine model, how air triggers inflammation and activation of complement and coagulation and their cross-talk.</p

Real-time feedback on chest compression efficacy by hands-free carotid Doppler in a porcine model

Aim: Current guidelines for cardiopulmonary resuscitation (CPR) recommend a one-size-fits-all approach in relation to the positioning of chest compressions. We recently developed RescueDoppler, a hands-free Doppler ultrasound device for continuous monitoring of carotid blood flow velocity during CPR. The aim of the present study is to investigate whether RescueDoppler via real-time hemodynamic feedback, could identify both optimal and suboptimal compression positions. Methods: In this model of animal cardiac arrest, we induced ventricular fibrillation in five domestic pigs. Manual chest compressions were performed for ten seconds at three different positions on the sternum in random order and repeated six times. We analysed Time Average Velocity (TAV) with chest compression position as a fixed effect and animal, position, and sequential time within animals as random effects. Furthermore, we compared TAV to invasive blood pressure from the contralateral carotid artery. Results: We were able to detect changes in TAV when altering positions. The positions with the highest (range 19 to 48 cm/s) and lowest (6–25 cm/s) TAV were identified in all animals, with corresponding peak pressure 50–81 mmHg, and 46–64 mmHg, respectively. Blood flow velocity was, on average, highest at the middle position (TAV 33 cm/s), but with significant variability between animals (SD 2.8) and positions within the same animal (SD 9.3). Conclusion: RescueDoppler detected TAV changes during CPR with alternating chest compression positions, identifying the position yielding maximal TAV. Future clinical studies should investigate if RescueDoppler can be used as a real-time hemodynamical feedback device to guide compression position

Hands-free continuous carotid Doppler ultrasound for detection of the pulse during cardiac arrest in a porcine model

Background/Purpose: Pulse palpation is an unreliable method for diagnosing cardiac arrest. To address this limitation, continuous hemodynamic monitoring may be a viable solution. Therefore, we developed a novel, hands-free Doppler system, RescueDoppler, to detect the pulse continuously in the carotid artery. Methods: In twelve pigs, we evaluated RescueDoppleŕs potential to measure blood flow velocity in three situations where pulse palpation of the carotid artery was insufficient: (1) systolic blood pressure below 60 mmHg, (2) ventricular fibrillation (VF) and (3) pulseless electrical activity (PEA). (1) Low blood pressure was induced using a Fogarty balloon catheter to occlude the inferior vena cava. (2) An implantable cardioverter-defibrillator induced VF. (3) Myocardial infarction after microembolization of the left coronary artery caused True-PEA. Invasive blood pressure was measured in the contralateral carotid artery. Time-averaged blood flow velocity (TAV) in the carotid artery was related to mean arterial pressure (MAP) in a linear mixed model. Results: RescueDoppler identified pulsatile blood flow in 41/41 events with systolic blood pressure below 60 mmHg, with lowest blood pressure of 19 mmHg. In addition the absence of spontaneous circulation was identified in 21/21 VF events and true PEA in 2/2 events. The intraclass correlation coefficient within animals for TAV and MAP was 0.94 (95% CI. 0.85–0.98). Conclusions: In a porcine model, RescueDoppler reliably identified pulsative blood flow with blood pressures below 60 mmHg. During VF and PEA, circulatory arrest was rapidly and accurately demonstrated. RescueDoppler could potentially replace unreliable pulse palpation during cardiac arrest and cardiopulmonary resuscitation