Fatal cerebral arterial gas embolism after endoscopic retrograde cholangiopancreatography

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Abstract

We report the case of a 50-year-old woman undergoing elective endoscopic retrograde cholangiopancreatography, who developed coma and hemiparesis secondary to severe cerebral artery gas embolism. Despite prompt diagnosis and early hyperbaric oxygen therapy (HBO ₂) she developed severe cerebral edema and died within 24 h.

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Most cited references 18

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Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts.

Terje Hagen, Thomas W D Edwards, D Scholz (1983)

The incidence and size of the patent foramen ovale were studied in 965 autopsy specimens of human hearts, which were from subjects who were evenly distributed by sex and age. Neither incidence nor size of the defect was significantly different between male and female subjects. The overall incidence was 27.3%, but it progressively declined with increasing age from 34.3% during the first three decades of life to 25.4% during the 4th through 8th decades and to 20.2% during the 9th and 10th decades. Among the 263 specimens that exhibited patency in our study, the foramen ovale ranged from 1 to 19 mm in maximal potential diameter (mean, 4.9 mm). In 98% of these cases, the foramen ovale was 1 to 10 mm in diameter. The size tended to increase with increasing age, from a mean of 3.4 mm in the first decade to 5.8 mm in the 10th decade of life.

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Cerebral air embolism resulting from invasive medical procedures. Treatment with hyperbaric oxygen.

Patrick B. Murphy, Julia F. Cramer, F Harford (1985)

The introduction of air into the venous or arterial circulation can cause cerebral air embolism, leading to severe neurological deficit or death. Air injected into the arterial circulation may have direct access to the cerebral circulation. A patent foramen ovale provides a right-to-left shunt for venous air to embolize to the cerebral arteries. The ability of the pulmonary vasculature to filter air may be exceeded by bolus injections of large amounts of air. Sixteen patients underwent hyperbaric oxygen therapy for cerebral air embolism. Neurological symptoms included focal motor deficit, changes in sensorium, and visual and sensory deficits. Eight patients (50%) had complete relief of symptoms as a result of hyperbaric treatment, five (31%) had partial relief, and three patients (19%) had no benefit, two of whom died. The treatment of cerebral air embolism with hyperbaric oxygen is based upon mechanical compression of air bubbles to a much smaller size and the delivery of high doses of oxygen to ischemic brain tissue.

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Cerebral arterial gas embolism following diagnostic bronchoscopy: delayed treatment with hyperbaric oxygen.

John Mehran, André D Beaulieu, C Wherrett (2001)

To describe a clinical scenario consistent with the diagnosis of cerebral arterial gas embolism (CAGE) acquired during an outpatient bronchoscopy. Our discussion explores the mechanisms and diagnosis of CAGE and the role of hyperbaric oxygen therapy. A diagnostic bronchoscopy was performed on a 70-yr-old man who had had a lobectomy for bronchogenic carcinoma three months earlier. During the direct insufflation of oxygen into the right middle lobe bronchus, the patient became unresponsive and developed subcutaneous emphysema. Immediately, an endotracheal tube and bilateral chest tubes were placed with resultant improvement in his oxygen saturation. However, he remained unresponsive with extensor and flexor responses to pain. Later, in the intensive care unit, he exhibited seizure activity requiring anticonvulsant therapy. Sedation was utilized only briefly to facilitate controlled ventilation. Investigations revealed a negative computerized tomography (CT) scan of the head, a normal cerebral spinal fluid examination, a CT chest that showed evidence of barotrauma, and an abnormal electroencephalogram. Fifty-two hours after the event, he was treated for presumed CAGE with hyperbaric oxygen using a modified United States Navy Table 6. Twelve hours later he had regained consciousness and was extubated. He underwent two more hyperbaric treatments and was discharged from hospital one week after the event, fully recovered. A patient with presumed CAGE made a complete recovery following treatment with hyperbaric oxygen therapy even though it was initiated after a significant time delay.

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Author and article information

Journal

Journal ID (nlm-ta): Indian J Crit Care Med

Journal ID (publisher-id): IJCCM

Title: Indian Journal of Critical Care Medicine : Peer-reviewed, Official Publication of Indian Society of Critical Care Medicine

Publisher: Medknow Publications (India )

ISSN (Print): 0972-5229

ISSN (Electronic): 1998-359X

Publication date (Print): Apr-Jun 2009

Volume: 13

Issue: 2

Pages: 108-112

Affiliations

From: [1 ]Columbia Asia Referral Hospital, Yeshwantpur, Bangalore - 560 055, India

Royal Adelaide Hospital, Adelaide, SA-5000

Author notes

Correspondence: Dr Pradeep Rangappa, Columbia Asia Referral Hospital, Yeshwantpur, Bangalore - 560 055, India. E-mail: drpradeepr@ 123456aol.com

Article

Publisher ID: IJCCM-13-108

DOI: 10.4103/0972-5229.56061

PMC ID: 2772239

PubMed ID: 19881196

SO-VID: d245163b-de17-4b24-99ea-673e0a85314e

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Fatal cerebral arterial gas embolism after endoscopic retrograde cholangiopancreatography

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Abstract

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Irish Journal of Paramedicine

Most cited references 18

Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts.

Cerebral air embolism resulting from invasive medical procedures. Treatment with hyperbaric oxygen.

Cerebral arterial gas embolism following diagnostic bronchoscopy: delayed treatment with hyperbaric oxygen.

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