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Venous Air Embolism, Result- Retrospective Study of Patients with Venous Or Arterial Ing in Prompt Hemodynamic Improvement

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Venous Air Embolism, Result- Retrospective Study of Patients with Venous Or Arterial Ing in Prompt Hemodynamic Improvement Ⅵ REVIEW ARTICLE David C. Warltier, M.D., Ph.D., Editor Anesthesiology 2007; 106:164–77 Copyright © 2006, the American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc. Diagnosis and Treatment of Vascular Air Embolism Marek A. Mirski, M.D., Ph.D.,* Abhijit Vijay Lele, M.D.,† Lunei Fitzsimmons, M.D.,† Thomas J. K. Toung, M.D.‡ exogenously delivered gas) from the operative field or This article has been selected for the Anesthesiology CME Program. After reading the article, go to http://www. other communication with the environment into the asahq.org/journal-cme to take the test and apply for Cate- venous or arterial vasculature, producing systemic ef- gory 1 credit. Complete instructions may be found in the fects. The true incidence of VAE may be never known, CME section at the back of this issue. much depending on the sensitivity of detection methods used during the procedure. In addition, many cases of Vascular air embolism is a potentially life-threatening event VAE are subclinical, resulting in no untoward outcome, that is now encountered routinely in the operating room and and thus go unreported. Historically, VAE is most often other patient care areas. The circumstances under which phy- associated with sitting position craniotomies (posterior sicians and nurses may encounter air embolism are no longer fossa). Although this surgical technique is a high-risk limited to neurosurgical procedures conducted in the “sitting procedure for air embolism, other recently described position” and occur in such diverse areas as the interventional radiology suite or laparoscopic surgical center. Advances in circumstances during both medical and surgical thera- monitoring devices coupled with an understanding of the peutics have further increased concern about this ad- pathophysiology of vascular air embolism will enable the phy- verse event. Conditions during which air embolism has sician to successfully manage these potentially challenging clin- been documented have substantively broadened, and ical scenarios. A comprehensive review of the etiology and much of the credit is owed to Albin et al.1–4 for their diagnosis of vascular air embolism, including approaches to prevention and management based on experimental and clini- description of the pathophysiology during a variety of cal data, is presented. This compendium of information will surgical procedures. Not only does the historic modus permit the healthcare professional to rapidly assess the relative operandi of a gravitational gradient remain a concern, risk of vascular air embolism and implement monitoring and but we must now as well be suspicious of VAE during treatment strategies appropriate for the planned invasive pro- modern procedures where gas may be entrained under cedure. pressure, both within the peritoneal cavity or via vascu- INTRAOPERATIVE vascular air embolism (VAE) was re- lar access. Hence, it is imperative for anesthesiologists to ported as early as the 19th century, in both pediatric and be aware of the causes of VAE, its morbidity, diagnostic adult practice. Well over 4,000 articles have been pub- considerations, treatment options, and adoption of prac- lished during the past 30 yr alone, providing ample tice patterns that best lead to the prevention of this resonance to the ubiquity and seriousness of this vascu- potentially fatal condition. lar event. Perhaps the most striking feature accumulated during this period is the myriad of clinical circumstances in which VAE may present itself, a result primarily of the Pathophysiology increased technological complexity and invasiveness of modern therapeutics. Most episodes of VAE are likely The two fundamental factors determining the morbid- preventable. This article provides a systematic review of ity and mortality of VAE are directly related to the vol- the pathophysiology and clinical presentation of this ume of air entrainment and rate of accumulation. When acute phenomenon, as well as an in-depth analysis and dealing simply with air being suctioned by a gravitational algorithms for favorable methods of detection, preven- gradient, these variables are mainly impacted by the tion, and treatment. position of the patient and height of the vein with Vascular air embolism is the entrainment of air (or respect to the right side of the heart. Experimental stud- ies have been conducted using several animal models to assess the volume of VAE necessary to provoke circula- * Associate Professor, † Fellow in Anesthesiology, ‡ Professor. tory collapse. Lethal volumes of air entrained as an acute Received from the Neurosciences Critical Care Division, Department of Anes- thesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Balti- bolus have been concluded to be approximately 0.5– more, Maryland. Submitted for publication November 24, 2003. Accepted for 0.75 ml/kg in rabbits5 and 7.5–15.0 ml/kg in dogs.6,7 publication August 23, 2006. Support was provided solely from institutional and/or departmental sources. Translating such data into the adult human would be Address correspondence to Dr. Mirski: Department of Anesthesiology and difficult, if not for some parallel confirmation from the Critical Care Medicine, 600 North Wolfe Street, Meyer Building 8-140, Baltimore, Maryland 21287. [email protected]. Individual article reprints may be accessed clinical literature. From case reports of accidental intra- 8,9 at no charge through the Journal Web site, www.anesthesiology.org. vascular delivery of air, the adult lethal volume has Anesthesiology, V 106, No 1, Jan 2007 164 VASCULAR AIR EMBOLISM 165 been described as between 200 and 300 ml, or 3–5 heart failure and immediate cardiovascular collapse. ml/kg. The authors of these reports suggest that the With more modest volumes of VAE, the embolism may closer the vein of entrainment is to the right heart, the still result in significant right ventricular outflow obstruc- smaller the required lethal volume is. tion, with an attendant decrease in cardiac output, hy- The rate of air entrainment is also of importance, potension, myocardial and cerebral ischemia, and even because the pulmonary circulation and alveolar interface death. Even if the cardiac output remains above that provide for a reservoir for dissipation of the intravascular required for adequate perfusion, the embolism may gas. As early as 1969, it was shown by Flanagan et al.10 nonetheless impart significant and even lethal injury. Air that a pressure decrease of 5 cm H2O across a 14-gauge entrainment into the pulmonary circulation may lead to needle (internal diameter of 1.8 mm) is capable of trans- pulmonary vasoconstriction, release of inflammatory me- mitting approximately 100 ml of air/s. This rate of en- diators, bronchoconstriction, and an increase in ventila- trainment easily exceeds lethal accumulation if not ter- tion/perfusion mismatch. minated immediately. Such data highlights the risk of catastrophic VAE in many vascular procedures per- formed in patients, because the luminal size is well Clinical Presentation within the diameter of commonly placed hardware. If entrainment is slow, the heart may be able to withstand Vascular air embolism may have cardiovascular, pul- large quantities of air despite entrainment over a pro- monary, and neurologic sequelae. The spectrum of ef- longed period. As shown by Hybels,11 dogs were able to fects is dependent on the rate and entrained volume of withstand up to 1,400 ml of air over a several-hour VAE, as well as other two additional factors: whether the period. patient is spontaneously breathing, yielding negative Both volume and rate of air accumulation are depen- thoracic pressure during respiratory cycle with facilita- dent on the size of the vascular lumen as well as the tion of air entrainment, or under controlled positive- pressure gradient. The risk of VAE is also present under pressure ventilation. An informative summary of the circumstances that prevent the collapse of veins even at common relation between clinical presentation and modest decreases of pressure relative to that in the acute embolism volume is presented in figure 1. venous system (surgical dissection). Not only negative Cardiovascularly, tachyarrhythmias are common, and pressure gradients but also positive pressure insufflation the electrocardiogram demonstrates a right heart strain of gas may present a serious VAE hazard. Injection of gas pattern as well as ST–T changes. Myocardial ischemia (or liquid–air mixtures), such as into the uterine cavity may be observed, and in animal studies, peaking of the P for separation of placental membrane or for a variety of wave is seen in the earlier stages. Blood pressure de- laparoscopic procedures, poses a risk for VAE. creases as cardiac output falters. Pulmonary artery pres- Early animal experiments indicated that VAE increases sures increase as a consequence of increased filling pres- microvascular permeability.12 Embolization of the right sures and reduction of cardiac output. The central ventricular chamber has been shown to induce pulmo- venous pressure measurements also increase as a sec- nary hypertension related to the release of endothelin 1 ondary effect of right heart failure, and jugular venous from the pulmonary vasculature.13 The microbubbles distension may be noted. As hypotension increases, formed due to turbulent flow in the circulation precipi- shock ensues. tate platelet aggregation and the release of platelet acti- Pulmonary symptoms in awake patients include acute vator inhibitor. This, in turn, may lead
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