Cerebral air embolism treated by pressure and hyperbaric oxygen

Catron, Philip W.; Dutka, A. J.; Biondi, David; Flynn, ET; Hallenbeck, John M.

doi:10.1212/wnl.41.2_part_1.314

Cited by 20 publications

(7 citation statements)

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“…Generally, those patients who received early therapy had a more favorable outcome. 5,8 Some of the patients with air embolism did not receive HBO therapy, and likewise, we found that such reported cases tended to have poor outcomes. 1,2,9,10 Immediate therapy with HBO is the treatment of choice for CAE.…”

Section: Discussionsupporting

confidence: 55%

Diffuse Cerebral Air Embolism Treated With Hyperbaric Oxygen: A Case Report

Fowler

2005

Journal of Neuroimaging

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A 54-year-old woman presented for cardiac evaluation of atypical chest pain. Workup included coronary angiography and a left ventriculogram, during which air was inadvertently injected, resulting in the development of an acute right hemisphere syndrome. Right carotid angiography was immediately performed, yielding only a delayed diffuse venous phase without focal vessel cutoffs. Within 60 minutes, the patient underwent hyperbaric oxygen therapy for the suspected cerebral air emboli. After removal from the chamber for technical reasons, she had a generalized tonic-clonic seizure, and further hyperbaric oxygen therapy was withheld. Initial computed tomography imaging obtained approximately 8 hours after symptom onset showed signs of early right hemispheric edema. Subsequent magnetic resonance imaging studies were markedly abnormal and suggestive of diffuse bilateral but predominantly right-sided parietal lobe edema with mildly positive diffusion-weighted imaging. Follow-up magnetic resonance imaging at 6 months was normal, and the patient's neurological examination returned to normal.

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Section: Discussionsupporting

confidence: 55%

Diffuse Cerebral Air Embolism Treated With Hyperbaric Oxygen: A Case Report

Fowler

2005

Journal of Neuroimaging

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“…8 The phenomenon of secondary deterioration is not confined to hyperbarically treated air embolism as a result of diving accidents, however, since it has been observed in iatrogenic cases with delayed therapy and occurs after apparent spontaneous recovery from air embolism. 7 - 9 Any therapy that could be shown to reduce the severity or incidence of secondary deterioration when used in combination with hyperbaric oxygen would be potentially useful in the treatment of victims of air embolism.…”

Section: >2mentioning

confidence: 99%

Effect of lidocaine on somatosensory evoked response and cerebral blood flow after canine cerebral air embolism.

Dutka

Mink

McDermott

et al. 1992

Stroke

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Background and Purpose: Victims of air embolism often recover rapidly on hyperbaric treatment then deteriorate again, even if hyperbaric treatment is continued. In previous animal experiments, lidocaine has been shown to improve recovery of somatosensory evoked response amplitude after air embolism. However, animals in these experiments rarely deteriorated. We have shown that the induction of air embolism and transient hypertension in canines produces deterioration despite hyperbaric treatment, and we decided to test the effect of lidocaine on somatosensory evoked potential recovery and cerebral blood flow in this model.Methods: Dogs were treated with repeated doses of lidocaine or equivalent volumes of saline during hyperbaric therapy after internal carotid air embolism and transient hypertension. The investigators were unaware of treatment group assignment during the experiments. The amplitude of the median nerve somatosensory evoked potential and cerebral blood flow measured with carbon-14-labeled iodoantipyrine autoradiography were used to assess effect of therapy.Results: Lidocaine-treated dogs recovered 60±10% (mean±95% confidence limits) of the baseline somatosensory evoked potential amplitude 220 minutes after air embolism; saline-treated dogs recovered 32±10% (a significant difference atp<0.01). Lidocaine-treated dogs also had higher cerebral blood flow values than saline-treated dogs 220 minutes after air embolism.Conclusions: Lidocaine ameliorated the delayed deterioration of evoked potential associated with air embolism and hypertension in this canine model. The improved cerebral blood flow may be a mechanism of action of lidocaine or an associated effect of improved neuronal survival. (Stroke 1992;23:1515-1521 KEY WORDS • cerebral blood flow • embolism • evoked potentials, somatosensory • lidocaine • dogs

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“…The first CT scan revealed air emboli in the high frontoparietal regions. A subsequent scan showed resorption of the air bubbles, stressing the efficacy of hyperbaric oxygen in patients with air embolism 5 . Watershed infarcts occurred as a result of the vulnerability of these areas to hypoxia in the event of vascular compromise.…”

Section: Discussionmentioning

confidence: 92%

Fatal cerebral air embolism as a complication of transbronchoscopic lung biopsy: A case report

Shetty

Fatterpekar

Manohar

et al. 2001

Australasian Radiology

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A rare complication of transbronchoscopic lung biopsy, namely a cerebral air embolism, is presented. The course of events following the embolic episode in the form of a fall in blood pressure, bradycardia and convulsions is documented, as is the presence of an air emboli on the CT scan of the brain with subsequent resorption of the emboli on the follow-up scan. The salient features of the case are the rarity of the complication and the excellent temporal depiction of imaging findings on CT scan demonstrated as resorption of air emboli and subsequent watershed territory infarcts.

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Cerebral air embolism treated by pressure and hyperbaric oxygen

Cited by 20 publications

References 0 publications

Diffuse Cerebral Air Embolism Treated With Hyperbaric Oxygen: A Case Report

Diffuse Cerebral Air Embolism Treated With Hyperbaric Oxygen: A Case Report

Effect of lidocaine on somatosensory evoked response and cerebral blood flow after canine cerebral air embolism.

Fatal cerebral air embolism as a complication of transbronchoscopic lung biopsy: A case report

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