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CT pneumoangiogram sign following cardiopulmonary resuscitation: detrimental cerebral air embolism or postmortal blood replacement with air?
European Journal of Radiology Extra 45 (2003) 114 /117 http://intl.elsevierhealth.com/journals/ejrx
CT pneumoangiogram sign following cardiopulmonary resuscitation: detrimental cerebral air embolism or postmortal blood replacement with air? ¨ c¸o¨z, Ibrahim Somuncu Sahin Ugurel, Murat Kocaoglu, Mutlu Saglam *, Taner U Department of Radiology, Gu¨lhane Military Medical Academy, Ankara 06010, Turkey Received 17 June 2002; received in revised form 7 August 2002; accepted 9 August 2002
Abstract Massive air in the cerebral vessels (pneumoangiogram) on postmortal computed tomography (CT) examination after cardiopulmonary resuscitation of a 10-year-old child with severe thoracic trauma is reported and possible mechanism of pneumoangiogram is discussed. The patient suffered from severe head and chest injury and was transported to hospital in a cardiopulmonary arrest state. Cardiopulmonary resuscitation was not successful and to find the cause of death, postmortal cranial CT and supine chest X-radiography were performed. Chest X-ray revealed almost total obliteration of left pulmonary aeration as well as pneumomediastinum and bilateral hydropneumothorax. On CT scans, diffuse air was seen in the carotid arteries, middle and anterior cerebral arteries, the vertebral arteries, and in the right sigmoid sinus. This pneumoangiogram sign is believed to be the end result of pumped pneumothorax /pneumomediastinum air which was sucked through the lacerated thoracic great vessels via cardiac massage, replacing the emptied cerebral vessel lumens previously depleted of blood through massive thoracic hemorrhage and has nothing to do with a death contributing detrimental cerebral air embolism. # 2002 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Pneumoangiogram; Cerebral air embolism; Computed tomography; Cardiopulmonary resuscitation
1. Introduction
2. Case report
Cerebral air embolism has been described in several situations including cardiopulmonary resuscitation; however, computed tomography (CT) appearance varies from punctate air densities of the vasculature in mild cases to CT pneumoangiogram in massive ones [1 /4]. We report a case with CT pneumoangiogram following an unsuccessful posttraumatic cardiopulmonary resuscitation and claim a different mechanism than the previous authors for this CT finding.
A 10-year-old boy was brought to the emergency department after being run over by an automobile while he was cycling. Suffering from head and closed chest injury, he was apneic, pulseless and mydriatic on admission. After arrival to the critical care unit, he was intubated and vigorously ventilated by means of manual bag and closed heart massage was performed in association with intravenous epinephrine administration through a peripheral venous line. He did not recover and cardiopulmonary resuscitation was stopped an hour after admission. Since an autopsy permission could not be obtained, postmortal cranial CT scan was performed to find the causes of death, which in turn demonstrated diffuse air density areas located throughout both sides of the internal carotid arteries, vertebral arteries, middle cerebral and anterior cerebral arteries producing a pneumoangiogram of the anterior cerebral circulation (Fig. 1A /C). Skull fracture of the right temporal
* Corresponding author. Present address: GATA Lojmanlari, Serter Apt. No:9., 06120 Basinevleri, Ankara, Turkey. Tel.: /90-312-3043071; fax: /90-532-452-1840 E-mail address: [email protected] (M. Saglam).
1571-4675/03/$ - see front matter # 2002 Elsevier Science Ireland Ltd. All rights reserved. doi:10.1016/S1571-4675(03)00027-0
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Fig. 1. (A) Postmortal axial brain CT scan of the 10-year-old boy passing through Willis polligon demonstrates pneumoangiogram of anterior cerebral circulation and subcutaneous air bubbles and pneumocephalus neighboring right temporal squamous bone fracture region. (B) A lower level axial CT scan shows air in the petrous segment of the internal carotid artery, right sigmoid sinus (long arrow) and right infratemporal fossa (thick arrow). Besides, a minute pneumocephalus neighboring the right temporooccipital separation point (short arrow) is evident. (C) Lowest level axial CT scan passing through nasopharynx and atlas clearly depicts massive air in the retropharyngeal and carotid spaces (as an extension of pneumothorax) as well as the air bubbles totally filling the lumens of both side vertebral arteries (short arrows). Subcutaneous air bubbles in the right suboccipital region are also noted (long arrow).
squamous and occipital bones with pneumocephalus along with this region, soft tissue emphysema of the neighboring tissues, and air bubbles in the right sigmoid sinus and right infratemporal fossa were also observed (Fig. 1A,B). No air was seen in the basillary or posterior
cerebral arteries. Additionally, CT showed diffuse air density occupying the carotid and retropharyngeal space enveloping the carotid arteries and some subcutaneous air density bubbles in the suboccipital region (Fig. 1C). Cervical course of the internal juguler veins were not
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discernible. Besides, supine chest X-ray obtained postmortal was demonstrating a predominantly left-sided hydropneumothorax and pneumomediastinum associated with air density in the both side cervical common carotid artery traces. A few fractured ribs and parenchymal radioopacities consistent with hemorrhage were also noted.
3. Discussion Air access into the circulation can cause cerebral air embolism leading to severe neurological deficit or death [1]. Cerebral air embolism usually occurs either accidentally or iatrogenically, such as part of a decompression sickness and as a complication of numerous medical procedures including cardiopulmonary resuscitation, central line placement and intravenous therapy and needle biopsy of the lung [1 /3,5 /12]. Air bubbles can pass into arterial circulation or they can cross from venous circulation to the arterial system through pulmonary vessels via a physiological shunt (if it is excessive) or through cardiac septal defects [1,10 /12]. Cerebral air embolism during cerebral angiography might also be a frequent complication. However in many cases minute air is resorbed spontaneously either through cerebral tissue or through pulmonary capillary bed and that is why they are not diagnosed [5]. CT findings of cerebral air embolism may differ according to several factors, including the amount of air reaching cerebral vasculature and the timing of examination [2,3,8 /10]. In this case, no air was seen in the basillary and the posterior cerebral arteries, however, both vertebral arteries were pneumatized together with the anterior cerebral arterial circulation. In our opinion, pneumatization of different craniocerebral arteries in different amounts in several CT reports may also be explained by the preference of air distribution into external and internal carotid systems (in accordance with the anatomical bifurcation angle) or by the dependent portion of the head during the CT examinations. For this specific case, some air may have preferred the external carotid arterial system since negative air density areas were noted in the right infratemporal/ temporal fossae (maxillary and superficial temporal branches trace), and subcutaneous right suboccipital region (occipital branch trace), the latter two being possible end results of bone fractures as well. Due to the dependent position of the cerebellum and occipital lobes during the CT examination, pertaining intracranial arteries (basillary artery and its branches, as well as the posterior cerebral arteries) were devoid of air. Several authors have reported CT pneumoangiogram sign as an indicator of massive cerebral air embolism up to now. Several etiological mechanisms have been proposed for cerebral air embolism [2,4,6 /8,10 /12].
Hashimoto et al. [6] reported a case of massive cerebral air embolism followed by cardiopulmonary resuscitation in a traumatic patient. On postmortal cranial CT scans, air was seen only in the proximal parts of the main cerebral arteries. In the chest CT scans, severe haemopneumothorax associated with air densities in the right common carotid arteries, the heart and descending aorta was reported. They speculated that air entered the heart during artificial respiration by means of the shunt established between the major bronchus and the pulmonary veins after severe blunt chest trauma. It was thought that air pushed into the cranial arteries after closed heart massage. Iwama et al. [4] reported cerebral CT findings similar to those reported by Hashimoto et al. In that case the patient was transferred to the hospital in a cardiovascular arrest state. However the patient did not suffer from cardiopulmonary injury, and cardiopulmonary resuscitation succeeded. Air was thought to have been sucked into an injured sigmoid sinus and traveled to the left heart by means of traumatic bronchovenous shunt; then, cerebral air embolism occurred via systemic circulation. Imanishi et al. [11] suggested a ‘thoracic pump’ theory in which gas entering a venous line could be ejected into the cerebral veins retrogradely during cardiopulmonary resuscitation. They also concluded that if there were any right-to-left shunt such as patent foramen ovale and atrial septal defect, these could cause arterial air embolism. Butler and Hills [13] demonstrated that although the lung can filter the air bubbles effectively, oxygen toxicity and excessive volume of gas may lead to passage of venous air through the pulmonary vasculature and can result in arterial embolization in patients with nondefective hearts. In our patient, it might be reasonable to suppose the occurrence of one or more of these mechanisms, i.e. the air in the systemic circulation might have originated either from the pulmonary barotrauma or from the right sigmoid sinus air which was sucked by a traumatic window. However, since the amount of intravascular air is too much, it makes more sense to assume that this large amount of air entered the venous circulation via a traumatic shunt within the lung due to the traffic accident, thereafter to the cranial arterial circulation by the mechanical force of closed chest massage (Fig. 2). Unique aspect of our case was existence of air in the carotid and vertebral arteries in addition to the middle and anterior cerebral arteries, right sigmoid sinus and right jugular bulbus. Our case also showed pneumomediastinum and predominantly left sided hydropneumothorax in chest roentgenogram, presumably due to hemorrhage and barotrauma, in addition to rib fractures resulting from cardiopulmonary resuscitation procedure and chest trauma. Air involving the carotid and retropharyngeal spaces was demonstrated to be an extension of mediastinal emphysema on chest X-ray.
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blood; that air was sucked from the traumatically pneumatized thoracic cavity through the lacerated great vessels and was pumped via cardiac massage to the brain. It still deserves mentioning that cerebral air embolism may be more frequent than presumed in the patients suffering from severe cardiopulmonary thoracic injury if they are exposed to a subsequent cardiac massage and it should be adequately avoided as much as possible.
References
Fig. 2. The left posterior oblique diagram of thorax demonstrates how the thoracic and mediastinal air entered systemic circulation by the pulmonary veins and left heart chambers (arrows) due to increased intrathoracic pressure during external cardiac massage.
Due to the diffuse air density, internal jugular veins were not visualized individually. This massive amount of air introduced to vasculature suggests that pneumoangiography observed here is simply an influx of pumped air into the empty vessels which previously bled and poured their blood content into the thoracic cavity; i.e. it is not one of the primary contributors of death. In our opinion, the patient had died of hypovolemic shock and/or cerebral trauma at first place. It should be kept in mind that the mortality and morbidity of venous or arterial air embolism are related to volume of air, the patient’s cardiopulmonary status and rate of air flow. In humans mortality has been reported with injection of up to 100 /300 ml of air by peripheral venous line [14], however, a few milliliters of air injected into the pulmonary veins is fatal enough, as a consequence of coronary or cerebral vasculature obstruction [10]. In conclusion, some of cerebral CT pneumoangiograms following cardiopulmonary resuscitation reported up to now doubtfully represent real cases of fatal cerebral air embolism but rather, represent the post-mortal filling of vessel lumens with air replacing
[1] Murphy BP, Harford FJ, Cramer FS. Cerebral air embolism resulting from invasive medical procedures. Treatment with hyperbaric oxygen. Ann Surg 1985;201:242 /5. [2] Yamaki T, Ando S, Ohta K, Kubota T, Kawasaki K, Hirama M. CT demonstration of massive cerebral air embolism from pulmonary barotrauma due to cardiopulmonary resuscitation. J Comput Assist Tomogr 1989;13:313 /5. [3] Muras I, Bonsignore R, Cesaro L, Frascadore L, Bernini FP. Post-traumatic cerebral air embolism. J Neuroradiol 1994;21:267 /9. [4] Iwama T, Andoh H, Murase S, Miwa Y, Ohkuma A. Diffuse cerebral air embolism following trauma: striking postmortem CT findings. Neuroradiology 1994;36:33 /4. [5] Voorhies RM, Fraser RAR. Cerebral air embolism occurring at angiography and diagnosed by computerized tomography. J Neurosurg 1984;60:177 /8. [6] Hashimoto Y, Yamaki T, Sakakibara T, Matsui J, Matsui M. Cerebral air embolism caused by cardiopulmonary resuscitation after cardiopulmonary arrest on arrival. J Trauma 2000;48:975 /7. [7] Shiina G, Shimosegawa Y, Kameyama M, Onuma T. Massive cerebral air embolism following cardiopulmonary resuscitatiton. Report of two cases. Acta Neurochir (Wien) 1993;125:181 /3. [8] Akaishi K, Hongo K, Obinata C, Kobayashi S. Pneomoangiogram in a patient with severe head injury. J Neurosurg 2000;92:502. [9] Baker BK, Awwad EE. Computed tomography of fatal cerebral air embolism following percutaneous aspiration biopsy of the lung. J Comput Assist Tomogr 1988;12:1082 /3. [10] Cianci P, Posin JP, Shimshak RR, Singzon J. Air embolism complicating thin needle biopsy of the lung. Chest 1987;92:749 / 50. [11] Imanishi M, Nishimura A, Tabuse H, Miyamoto S, Sakaki T, Iwasaki S. Intracranial gas on CT after cardiopulmonary resuscitation: 4 cases. Neuroradiology 1998;40:154 /7. [12] Jensen ME, Lipper MH. CT in iatrogenic cerebral air embolism. Am J Neuroradiol 1986;7:823 /7. [13] Butler BD, Hills BA. The lung as a filter for microbubbles. J Appl Physiol 1979;47:537 /43. [14] Yeakel AE. Lethal air embolism from plastic blood-storage container. J Am Med Assoc 1968;204:267 /9.
CT pneumoangiogram sign following cardiopulmonary resuscitation: detrimental cerebral air embolism or postmortal blood replacement with air? ¨ c¸o¨z, Ibrahim Somuncu Sahin Ugurel, Murat Kocaoglu, Mutlu Saglam *, Taner U Department of Radiology, Gu¨lhane Military Medical Academy, Ankara 06010, Turkey Received 17 June 2002; received in revised form 7 August 2002; accepted 9 August 2002
Abstract Massive air in the cerebral vessels (pneumoangiogram) on postmortal computed tomography (CT) examination after cardiopulmonary resuscitation of a 10-year-old child with severe thoracic trauma is reported and possible mechanism of pneumoangiogram is discussed. The patient suffered from severe head and chest injury and was transported to hospital in a cardiopulmonary arrest state. Cardiopulmonary resuscitation was not successful and to find the cause of death, postmortal cranial CT and supine chest X-radiography were performed. Chest X-ray revealed almost total obliteration of left pulmonary aeration as well as pneumomediastinum and bilateral hydropneumothorax. On CT scans, diffuse air was seen in the carotid arteries, middle and anterior cerebral arteries, the vertebral arteries, and in the right sigmoid sinus. This pneumoangiogram sign is believed to be the end result of pumped pneumothorax /pneumomediastinum air which was sucked through the lacerated thoracic great vessels via cardiac massage, replacing the emptied cerebral vessel lumens previously depleted of blood through massive thoracic hemorrhage and has nothing to do with a death contributing detrimental cerebral air embolism. # 2002 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Pneumoangiogram; Cerebral air embolism; Computed tomography; Cardiopulmonary resuscitation
1. Introduction
2. Case report
Cerebral air embolism has been described in several situations including cardiopulmonary resuscitation; however, computed tomography (CT) appearance varies from punctate air densities of the vasculature in mild cases to CT pneumoangiogram in massive ones [1 /4]. We report a case with CT pneumoangiogram following an unsuccessful posttraumatic cardiopulmonary resuscitation and claim a different mechanism than the previous authors for this CT finding.
A 10-year-old boy was brought to the emergency department after being run over by an automobile while he was cycling. Suffering from head and closed chest injury, he was apneic, pulseless and mydriatic on admission. After arrival to the critical care unit, he was intubated and vigorously ventilated by means of manual bag and closed heart massage was performed in association with intravenous epinephrine administration through a peripheral venous line. He did not recover and cardiopulmonary resuscitation was stopped an hour after admission. Since an autopsy permission could not be obtained, postmortal cranial CT scan was performed to find the causes of death, which in turn demonstrated diffuse air density areas located throughout both sides of the internal carotid arteries, vertebral arteries, middle cerebral and anterior cerebral arteries producing a pneumoangiogram of the anterior cerebral circulation (Fig. 1A /C). Skull fracture of the right temporal
* Corresponding author. Present address: GATA Lojmanlari, Serter Apt. No:9., 06120 Basinevleri, Ankara, Turkey. Tel.: /90-312-3043071; fax: /90-532-452-1840 E-mail address: [email protected] (M. Saglam).
1571-4675/03/$ - see front matter # 2002 Elsevier Science Ireland Ltd. All rights reserved. doi:10.1016/S1571-4675(03)00027-0
S. Ugurel et al. / European Journal of Radiology Extra 45 (2003) 114 /117
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Fig. 1. (A) Postmortal axial brain CT scan of the 10-year-old boy passing through Willis polligon demonstrates pneumoangiogram of anterior cerebral circulation and subcutaneous air bubbles and pneumocephalus neighboring right temporal squamous bone fracture region. (B) A lower level axial CT scan shows air in the petrous segment of the internal carotid artery, right sigmoid sinus (long arrow) and right infratemporal fossa (thick arrow). Besides, a minute pneumocephalus neighboring the right temporooccipital separation point (short arrow) is evident. (C) Lowest level axial CT scan passing through nasopharynx and atlas clearly depicts massive air in the retropharyngeal and carotid spaces (as an extension of pneumothorax) as well as the air bubbles totally filling the lumens of both side vertebral arteries (short arrows). Subcutaneous air bubbles in the right suboccipital region are also noted (long arrow).
squamous and occipital bones with pneumocephalus along with this region, soft tissue emphysema of the neighboring tissues, and air bubbles in the right sigmoid sinus and right infratemporal fossa were also observed (Fig. 1A,B). No air was seen in the basillary or posterior
cerebral arteries. Additionally, CT showed diffuse air density occupying the carotid and retropharyngeal space enveloping the carotid arteries and some subcutaneous air density bubbles in the suboccipital region (Fig. 1C). Cervical course of the internal juguler veins were not
116
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discernible. Besides, supine chest X-ray obtained postmortal was demonstrating a predominantly left-sided hydropneumothorax and pneumomediastinum associated with air density in the both side cervical common carotid artery traces. A few fractured ribs and parenchymal radioopacities consistent with hemorrhage were also noted.
3. Discussion Air access into the circulation can cause cerebral air embolism leading to severe neurological deficit or death [1]. Cerebral air embolism usually occurs either accidentally or iatrogenically, such as part of a decompression sickness and as a complication of numerous medical procedures including cardiopulmonary resuscitation, central line placement and intravenous therapy and needle biopsy of the lung [1 /3,5 /12]. Air bubbles can pass into arterial circulation or they can cross from venous circulation to the arterial system through pulmonary vessels via a physiological shunt (if it is excessive) or through cardiac septal defects [1,10 /12]. Cerebral air embolism during cerebral angiography might also be a frequent complication. However in many cases minute air is resorbed spontaneously either through cerebral tissue or through pulmonary capillary bed and that is why they are not diagnosed [5]. CT findings of cerebral air embolism may differ according to several factors, including the amount of air reaching cerebral vasculature and the timing of examination [2,3,8 /10]. In this case, no air was seen in the basillary and the posterior cerebral arteries, however, both vertebral arteries were pneumatized together with the anterior cerebral arterial circulation. In our opinion, pneumatization of different craniocerebral arteries in different amounts in several CT reports may also be explained by the preference of air distribution into external and internal carotid systems (in accordance with the anatomical bifurcation angle) or by the dependent portion of the head during the CT examinations. For this specific case, some air may have preferred the external carotid arterial system since negative air density areas were noted in the right infratemporal/ temporal fossae (maxillary and superficial temporal branches trace), and subcutaneous right suboccipital region (occipital branch trace), the latter two being possible end results of bone fractures as well. Due to the dependent position of the cerebellum and occipital lobes during the CT examination, pertaining intracranial arteries (basillary artery and its branches, as well as the posterior cerebral arteries) were devoid of air. Several authors have reported CT pneumoangiogram sign as an indicator of massive cerebral air embolism up to now. Several etiological mechanisms have been proposed for cerebral air embolism [2,4,6 /8,10 /12].
Hashimoto et al. [6] reported a case of massive cerebral air embolism followed by cardiopulmonary resuscitation in a traumatic patient. On postmortal cranial CT scans, air was seen only in the proximal parts of the main cerebral arteries. In the chest CT scans, severe haemopneumothorax associated with air densities in the right common carotid arteries, the heart and descending aorta was reported. They speculated that air entered the heart during artificial respiration by means of the shunt established between the major bronchus and the pulmonary veins after severe blunt chest trauma. It was thought that air pushed into the cranial arteries after closed heart massage. Iwama et al. [4] reported cerebral CT findings similar to those reported by Hashimoto et al. In that case the patient was transferred to the hospital in a cardiovascular arrest state. However the patient did not suffer from cardiopulmonary injury, and cardiopulmonary resuscitation succeeded. Air was thought to have been sucked into an injured sigmoid sinus and traveled to the left heart by means of traumatic bronchovenous shunt; then, cerebral air embolism occurred via systemic circulation. Imanishi et al. [11] suggested a ‘thoracic pump’ theory in which gas entering a venous line could be ejected into the cerebral veins retrogradely during cardiopulmonary resuscitation. They also concluded that if there were any right-to-left shunt such as patent foramen ovale and atrial septal defect, these could cause arterial air embolism. Butler and Hills [13] demonstrated that although the lung can filter the air bubbles effectively, oxygen toxicity and excessive volume of gas may lead to passage of venous air through the pulmonary vasculature and can result in arterial embolization in patients with nondefective hearts. In our patient, it might be reasonable to suppose the occurrence of one or more of these mechanisms, i.e. the air in the systemic circulation might have originated either from the pulmonary barotrauma or from the right sigmoid sinus air which was sucked by a traumatic window. However, since the amount of intravascular air is too much, it makes more sense to assume that this large amount of air entered the venous circulation via a traumatic shunt within the lung due to the traffic accident, thereafter to the cranial arterial circulation by the mechanical force of closed chest massage (Fig. 2). Unique aspect of our case was existence of air in the carotid and vertebral arteries in addition to the middle and anterior cerebral arteries, right sigmoid sinus and right jugular bulbus. Our case also showed pneumomediastinum and predominantly left sided hydropneumothorax in chest roentgenogram, presumably due to hemorrhage and barotrauma, in addition to rib fractures resulting from cardiopulmonary resuscitation procedure and chest trauma. Air involving the carotid and retropharyngeal spaces was demonstrated to be an extension of mediastinal emphysema on chest X-ray.
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blood; that air was sucked from the traumatically pneumatized thoracic cavity through the lacerated great vessels and was pumped via cardiac massage to the brain. It still deserves mentioning that cerebral air embolism may be more frequent than presumed in the patients suffering from severe cardiopulmonary thoracic injury if they are exposed to a subsequent cardiac massage and it should be adequately avoided as much as possible.
References
Fig. 2. The left posterior oblique diagram of thorax demonstrates how the thoracic and mediastinal air entered systemic circulation by the pulmonary veins and left heart chambers (arrows) due to increased intrathoracic pressure during external cardiac massage.
Due to the diffuse air density, internal jugular veins were not visualized individually. This massive amount of air introduced to vasculature suggests that pneumoangiography observed here is simply an influx of pumped air into the empty vessels which previously bled and poured their blood content into the thoracic cavity; i.e. it is not one of the primary contributors of death. In our opinion, the patient had died of hypovolemic shock and/or cerebral trauma at first place. It should be kept in mind that the mortality and morbidity of venous or arterial air embolism are related to volume of air, the patient’s cardiopulmonary status and rate of air flow. In humans mortality has been reported with injection of up to 100 /300 ml of air by peripheral venous line [14], however, a few milliliters of air injected into the pulmonary veins is fatal enough, as a consequence of coronary or cerebral vasculature obstruction [10]. In conclusion, some of cerebral CT pneumoangiograms following cardiopulmonary resuscitation reported up to now doubtfully represent real cases of fatal cerebral air embolism but rather, represent the post-mortal filling of vessel lumens with air replacing
[1] Murphy BP, Harford FJ, Cramer FS. Cerebral air embolism resulting from invasive medical procedures. Treatment with hyperbaric oxygen. Ann Surg 1985;201:242 /5. [2] Yamaki T, Ando S, Ohta K, Kubota T, Kawasaki K, Hirama M. CT demonstration of massive cerebral air embolism from pulmonary barotrauma due to cardiopulmonary resuscitation. J Comput Assist Tomogr 1989;13:313 /5. [3] Muras I, Bonsignore R, Cesaro L, Frascadore L, Bernini FP. Post-traumatic cerebral air embolism. J Neuroradiol 1994;21:267 /9. [4] Iwama T, Andoh H, Murase S, Miwa Y, Ohkuma A. Diffuse cerebral air embolism following trauma: striking postmortem CT findings. Neuroradiology 1994;36:33 /4. [5] Voorhies RM, Fraser RAR. Cerebral air embolism occurring at angiography and diagnosed by computerized tomography. J Neurosurg 1984;60:177 /8. [6] Hashimoto Y, Yamaki T, Sakakibara T, Matsui J, Matsui M. Cerebral air embolism caused by cardiopulmonary resuscitation after cardiopulmonary arrest on arrival. J Trauma 2000;48:975 /7. [7] Shiina G, Shimosegawa Y, Kameyama M, Onuma T. Massive cerebral air embolism following cardiopulmonary resuscitatiton. Report of two cases. Acta Neurochir (Wien) 1993;125:181 /3. [8] Akaishi K, Hongo K, Obinata C, Kobayashi S. Pneomoangiogram in a patient with severe head injury. J Neurosurg 2000;92:502. [9] Baker BK, Awwad EE. Computed tomography of fatal cerebral air embolism following percutaneous aspiration biopsy of the lung. J Comput Assist Tomogr 1988;12:1082 /3. [10] Cianci P, Posin JP, Shimshak RR, Singzon J. Air embolism complicating thin needle biopsy of the lung. Chest 1987;92:749 / 50. [11] Imanishi M, Nishimura A, Tabuse H, Miyamoto S, Sakaki T, Iwasaki S. Intracranial gas on CT after cardiopulmonary resuscitation: 4 cases. Neuroradiology 1998;40:154 /7. [12] Jensen ME, Lipper MH. CT in iatrogenic cerebral air embolism. Am J Neuroradiol 1986;7:823 /7. [13] Butler BD, Hills BA. The lung as a filter for microbubbles. J Appl Physiol 1979;47:537 /43. [14] Yeakel AE. Lethal air embolism from plastic blood-storage container. J Am Med Assoc 1968;204:267 /9.