Letters COMMENT & RESPONSE

Cerebral Venous Air Embolism: What Is It and Do We Know How to Deal With It Properly? To the Editor Cerebral venous air embolism (CVAE) is reported more frequently and may be associated with poor neurological outcome or even mortality.1,2 It is often associated with certain iatrogenic procedures,2 in particular central venous access may play a major role in the incidence of this serious event.1,3-5 However, in contrast to cerebral arterial air embolism, awareness of CVAE is still lacking; its retrograde mechanism seems to be not fully understood and might therefore be grossly underreported.3,4 We would like to point out that once air bubbles enter the superior vena cava, the low specific weight of air bubbles in blood will always make them prone to rise cranially in a patient positioned upright, provided the air bubbles rise at a velocity that is greater than the velocity of the opposing blood flow in the vein. Laboratory investigations have demonstrated that air bubbles have a high probability of rising retrograde against venous blood flow; this depends on bubble size, central vein diameter, cardiac output, and the position of the patient’s head above the heart.4,5 With increasing overall crosssection of the feeding veins, the flow velocity in the peripheral vein decreases and facilitates retrograde rise of air bubbles to the brain. To our knowledge, current neuroscience literature still has not defined (retrograde) CVAE and its morphologic sequelae in the brain. Research should be emphasized on this topic. Furthermore, little is known on the emergency treatment for (retrograde) CVAE. The Trendelenburg position to induce air bubbles to leave the cerebral veins and return to central venous circulation seems reasonable in the initial stage but has not been studied or reported yet. The treatment of established neurological damage due to CVAE is probably hyperbaric oxygenation therapy (HBOT), but that would need further evaluation. With (retrograde) CVAE there is no immediate arterial obstruction causing ischemia. The inflammatory response between gas bubbles and the endothelium may lead to activation of neutrophils with β-2 integrin adhesion to endothelial cells, resulting in stasis and venous infarction. However, this biochemical process may potentially allow more time to arrange HBOT.3 Hyperbaric oxygenation therapy has been shown to be effective in a patient with CVAE3 in contrast to the recently reported case by Lai et al in JAMA Neurology.1 Therefore, detail regarding the interval between diagnoses and HBOT, as well as detail of the HBOT protocol, would be invaluable. Christoph J. Schlimp, MD Pieter A. Bothma, FCA(SA), MMed Andreas E. Brodbeck, MD jamaneurology.com

Author Affiliations: Ludwig Boltzmann for Experimental and Clinical Traumatology, AUVA Research Centre, Vienna, Austria (Schlimp); James Paget University Hospitals NHS Foundation Trust, Norfolk, England (Bothma, Brodbeck). Corresponding Author: Christoph J. Schlimp, MD, Ludwig Boltzmann for Experimental and Clinical Traumatology, AUVA Research Centre, Donaueschingenstrasse 13, A-1200 Vienna, Austria ([email protected] .lbg.ac.at). Conflict of Interest Disclosures: None reported. 1. Lai D, Jovin TG, Jadhav AP. Cortical vein air emboli with gyriform infarcts. JAMA Neurol. 2013;70(7):939-940. 2. Nern C, Bellut D, Husain N, Pangalu A, Schwarz U, Valavanis A. Fatal cerebral venous air embolism during endoscopic retrograde cholangiopancreatography: case report and review of the literature. Clin Neuroradiol. 2012;22(4):371-374. 3. Bothma PA, Brodbeck AE, Smith BA. Cerebral venous air embolism treated with hyperbaric oxygen: a case report. Diving Hyperb Med. 2012;42(2):101-103. 4. Schlimp CJ, Loimer T, Rieger M, Lederer W, Schmidts MB. The potential of venous air embolism ascending retrograde to the brain. J Forensic Sci. 2005;50(4):906-909. 5. Fracasso T, Karger B, Schmidt PF, Reinbold WD, Pfeiffer H. Retrograde venous cerebral air embolism from disconnected central venous catheter: an experimental model. J Forensic Sci. 2011;56(s1)(suppl 1):S101-S104.

In Reply We appreciate the insightful commentary from our colleagues, Schlimp et al, regarding our article on cerebral air embolism.1 Despite a lack of prospective data, emergent therapies focus on Trendelenburg patient positioning and hyperbaric oxygen treatment (HBOT). Moreover, the precise pathophysiology of cerebral venous air embolization has yet to be delineated. Nonetheless, the literature does provide a number of retrospective clinical observations and animal model studies on which we base our clinical decisions. Current therapies are relatively noninvasive, with low potential for major complications. Hyperbaric oxygen treatment may be considered in the care of air embolism particularly if therapy can be initiated in a timely fashion. A large air embolus capable of producing clinical neurologic symptoms can take several hours for resorption to occur. Animal models have demonstrated that HBOT acts by increasing the partial pressure of oxygen dissolved in the blood as well as reducing cerebral edema by denitrogenation of cerebral tissue.2 At our institution, we provided our patient described in the article with HBOT within 6 hours of symptom onset. We used the US Navy diving algorithm described in Table 6 in the article, which is specific for treatment of air embolism.3 Van Hulst et al2 presented 9 clinical retrospective studies of cases of cerebral air embolism treated with HBOT that demonstrated a range of outcomes: 8% to 33% mortality and 33% to 75% of patients had complete neurologic recovery. Prognostically, Heckman et al4 described a separate series in which they characterized the presentation of their patient as being focal (eg, aphasic or hemiparetic) or essentially nonfocal (eg, acute confusion or coma). The nonfocal group was observed to have a higher mortality rate than the focal group (36% vs JAMA Neurology February 2014 Volume 71, Number 2

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8%), although the authors noted a discrepancy in age difference between groups (64 years in the nonfocal group vs 44 years in the focal group). Animal model studies have shown that earlier treatment with HBOT decreases intracranial pressure and improves cerebral oxygenation levels.5 In combination with the observations by Heckman et al4 of a generally encephalopathic state portending a poorer outcome, it is possible that the causative pathophysiology of encephalopathy in the nonfocal group is related to increased intracranial pressure. Therefore, the effective therapeutic window of HBOT treatment may be clinically based (ie, prior to onset of encephalopathy for the affected patient). Daniel Lai, MD Ashutosh P. Jadhav, MD, PhD Author Affiliations: Department of Neurology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania (Lai, Jadhav). Corresponding Author: Ashutosh P. Jadhav, MD, PhD, Department of Neurology, University of Pittsburgh Medical Center, 3471 Fifth Ave, Kaufman Medical Building, Ste 81, Pittsburgh, PA 15213 ([email protected]). Conflict of Interest Disclosures: None reported. 1. Lai D, Jovin TG, Jadhav AP. Cortical vein air emboli with gyriform infarcts. JAMA Neurol. 2013;70(7):939-940. 2. van Hulst RA, Klein J, Lachmann B. Gas embolism: pathophysiology and treatment. Clin Physiol Funct Imaging. 2003;23(5):237-246.

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3. Defense Department, United States Navy, Naval Sea Systems Command. Diving Medicine & Recompression Chamber Operations: United States Diving Manual, Vol 5. Baton Rouge, LA: Claitor's Publishing Division; 2005:20-42. 4. Heckmann JG, Lang CJ, Kindler K, Huk W, Erbguth FJ, Neundörfer B. Neurologic manifestations of cerebral air embolism as a complication of central venous catheterization. Crit Care Med. 2000;28(5):1621-1625. 5. van Hulst RA, Drenthen J, Haitsma JJ, et al. Effects of hyperbaric treatment in cerebral air embolism on intracranial pressure, brain oxygenation, and brain glucose metabolism in the pig. Crit Care Med. 2005;33(4):841-846.

CORRECTION Incorrect Author Name: In the Original Investigation titled “Neuronal Surface and Glutamic Acid Decarboxylase Autoantibodies in Nonparaneoplastic Stiff Person Syndrome,” published online July 22, 2013, and in the September issue of JAMA Neurology (2013;70[9]:1140-1149. doi:10.1001/jamaneurol.2013.3499), an author’s name was given incorrectly in the byline (page 1140) and in the Author Affiliations and Author Contributions sections (page 1148). In the byline, the eighth author’s name should have been given as “Gabor Szabó, PhD.” In the Author Affiliations section, the fourth affiliation should have been listed as “Department of Gene Technology and Developmental Neurobiology, Institute of Experimental Medicine, Budapest, Hungary (Erdelyi, Szabó).” In the Author Contributions section, the list of authors contributing analysis and interpretation of data should have appeared as “Chang, Alexopoulos, Carvajal-González, Szabó, Vincent”; those contributing critical revision of the manuscript for important intellectual content should have appeared as “Chang, Alexopoulos, McMenamin, Carvajal-González, Alexander, Deacon, Szabó, Lang, Blaes, Brown, Vincent”; and those providing administrative, technical, and material support should have been given as “Chang, McMenamin, Alexander, Erdelyi, Szabó, Lang, Brown, Vincent.” This article was corrected online.

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