Massive Cerebral Air Embolism after Bronchoscopy and Central Line Manipulation
Joerg Seeburger, MD,
Michael A Borger, MD,
Denis R Merk, MD,
Susanne Doll, MD,
Hartmuth B Bittner, MD,
Friedrich W Mohr, MD
Heart Center, Leipzig University, Leipzig, Germany
Joerg Seeburger, MD, Tel: + 49 341 865 1421, Fax: + 49 341 865 1452, Email: j.seeburger{at}web.de, Heart Center, Leipzig University, Struempelstrasse 39, 04289 Leipzig, Germany.
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ABSTRACT
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A 50-year-old woman who underwent double-lung transplantation suffered a massive cerebral air embolism with severe neurological impairment and temporary hemodynamic deterioration after surveillance bronchoscopy and central line removal. We hypothesize that this was due to microscopic pulmonary parenchymal injury during bronchoscopy as well as air entrainment during removal of the central venous line, with subsequent transpulmonary passage into the cerebral vessels.
Key Words: Brain Infarction • Brain Injury • Chronic • Bronchoscopy • Embolism • Air
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INTRODUCTION
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Cerebral air embolism is a well-documented but rare complication of several medical procedures including bronchoscopy, lung biopsy, and central venous line insertion.1–3 Cerebral air embolism is associated with severe neurologic injury and poor outcomes.4 We describe an unusual case of cerebral air embolism following bronchoscopy and central venous line removal.
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CASE REPORT
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A 50-year-old woman with endstage lung emphysema underwent routine bilateral lung transplantation with an uneventful postoperative course. On postoperative day 12, surveillance bronchoscopy (Pentax FB-15B5, Hamburg, Germany) showed well-healing bronchial anastomoses and tissue, without any obvious abnormalities. Three hours later, the central venous catheter (Vygon MultiCath 5 Expert, Aachen, Germany) was removed from the right internal jugular vein with the patient lying supine in bed. Her head was elevated nearly 45° during this procedure, which was followed by application of continuous pressure over the wound. She was moved to her left side for routine nursing care 5 h later and suddenly developed seizure, gaze deviation to the right, left-sided hemiplegia, and unconsciousness. Her clinical status deteriorated rapidly, requiring hemodynamic resuscitative support and subsequent management in the intensive care unit. Computed tomography was immediately performed, which showed numerous intravascular air densities in the right cerebral hemisphere (Figure 1
, left). Transesophageal echocardiography excluded intracardiac defects and atherosclerosis in the ascending aorta and aortic arch. Five days later, the patient regained consciousness but continued to have left-sided hemiplegia. Magnetic resonance imaging 5 days after the event showed right cerebral infarction and post-ischemic cerebral edema (Figure 1, right). Subsequent intensive neurological rehabilitation was conducted. At six months postoperatively, there were persistent neurological deficits with left-sided hemiplegia.
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Figure 1. Air embolism in the right cerebral hemisphere documented by (left) computed tomography and (right) magnetic resonance imaging, showing right cerebral ischemia and edema five days after the acute event.
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DISCUSSION
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Cerebral air embolism has been reported during several medical procedures.1–6 We believe it was the cause of sudden severe neurological impairment in our patient because of the typical computed tomography and magnetic resonance imaging findings and the timing of the clinical events. Bronchoscopy and removal of a central venous catheter occurred prior to development of neurological symptoms; both have been documented as causes of cerebral air embolism. We believe the predominantly right-sided cerebral injury was a result of the patient being positioned on her left side at the time of the insult, making the right carotid artery more susceptible to air embolization. She also developed immediate hemodynamic instability that eventually resolved with supportive measures only. Such temporary hemodynamic instability is typical of coronary air embolism but unusual for cerebral atherosclerotic or thrombus embolization.7 Another reason why atherosclerotic embolism was an unlikely cause of neurologic injury in this case was the absence of aortic atherosclerosis on transesophageal echocardiography, computed tomography, and magnetic resonance imaging. An intracardiac cause of stroke was ruled out by transesophageal echocardiography.
Etiologically, cerebral air embolism requires two predisposing factors: entry of air into the circulation, and antegrade transport of the embolus to the cerebral vasculature. Diagnostic bronchoscopy has been reported to enable inflow of air to the circulation due to vessel trauma and parenchymal defects.1 Examination-related coughing during the procedure may increase intra-alveolar pressure, leading to barotrauma and passage of gas from the alveoli directly into the pulmonary venous circulation.2 Air in the pulmonary venous circulation can subsequently embolize to the cerebral vasculature with relative ease. Cerebral air embolism has also been described following systemic venous air entrapment, even in the absence of intracardiac defects.5 Entrainment of air in the venous system due to negative pressure after removal of a central venous catheter is a well-described but unusual complication of routine postoperative care.3 The exact mechanism whereby such systemic venous air reaches the cerebral vasculature in patients without intracardiac defects is unknown. One possible explanation is that the pulmonary venous microcirculation is overwhelmed and eventually traversed because air emboli can easily deform.4 Another is that an undiagnosed patent foramen ovale temporarily opens when pulmonary arterial pressure rises, analogous to cerebral fat embolization that can occur during hip surgery.6
We believe that continuous insufflation of small air volumes during bronchoscopy-related microscopic pulmonary tissue injury, combined with further accumulation of air caused by removal of the central venous catheter, was the probable source of intravascular air in our patient. The pulmonary tissue may have been particularly susceptible to air entrapment because of the post-transplantation inflammatory state of the pulmonary vasculature. Treatment of cerebral air embolism is mostly supportive in nature. Although some reports advocate hyperbaric therapy, there is no consensus on the efficacy of this modality.4 We did not apply hyperbaric therapy because of the lack of a hyperbaric chamber in our center and, more importantly, because of the patient’s hemodynamic instability immediately after the event. Cerebral air embolism is an uncommon but debilitating complication that should be considered in patients with sudden neurologic deterioration after bronchoscopy or central venous line manipulation.
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REFERENCES
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- Edmonds CR, Barbut D, Hager D, Sharrock NE. Intraoperative cerebral arterial embolization during total hip arthroplasty. Anesthesiology 2000;93:315–8.[Medline]
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Asian Cardiovasc Thorac Ann 2009;
17:67-69
© 2009 by SAGE Publications
DOI: 10.1177/0218492309102501
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ABSTRACT
INTRODUCTION
