Venous Air Embolism during Surgery, Especially Cesarean Delivery

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Venous air embolism (VAE) is the entrapment of air or medical gases into the venous system causing symptoms and signs of pulmonary vessel obstruction. The incidence of VAE during cesarean delivery ranges from 10 to 97% depending on surgical position or diagnostic tools, with a potential for life-threatening events. We reviewed extensive literatures regarding VAE in detail and herein described VAE during surgery including cesarean delivery from background and history to treatment and prevention. It is intended that present work will improve the understanding of VAE during surgery.

Related collections

Most cited references 86

Record: found
Abstract: found
Article: not found

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.

0 comments Cited 30 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

The pathophysiology of failure in acute right ventricular hypertension: hemodynamic and biochemical correlations.

G J Vlahakes, K Turley, J. Hoffman (1980)

Acute right ventricular (RV) hypertension and failure occur clinically. In this study we examined the mechanism of RV failure. Adult dogs were studied acutely under anesthesia; dogs were instrumented for measurement of pressures and right coronary artery blood flow. Myocardial blood flow and cardiac output were determined with radionuclide-labeled microspheres, and the presence of ischemia was determined by biochemical analysis of ventricular biopsies. RV hypertension was produced by constricting the pulmonary artery and was increased until RV failure occurred, as evidenced by decreased aortic pressure and cardiac output and increased RV end-diastolic pressure. With increasing RV systolic pressure, RV myocardial blood flow failed to increase in proportion to demand. At the onset of RV failure, there was no reactive hyperemia of right coronary flow compared with control, indicating the absence of further coronary vascular reserve; biochemical analysis demonstrated that the RV free wall was ischemic; the LV free wall was not. Infusion of phenylephrine raised aortic pressure and hence, myocardial perfusion pressure; RV failure reversed as shown by decreased RV end-diastolic pressure and increased cardiac output and RV systolic pressure; reactive hyperemia of right coronary flow was restored and the biochemical indexes of ischemia were reversed, demonstrating that ischemia is the cause of failure in acute RV hypertension.

0 comments Cited 27 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Systemic air embolism after lung trauma.

Kai Ho, A.-E. Ling (1999)

Systemic air or gas embolism has been increasingly recognized as a complication of serious chest trauma and often presents with catastrophic circulatory and cerebral events. The classic findings are hemoptysis, sudden cardiac or cerebral dysfunction after initiation of PPV, air in retinal vessels, and air in arterial aspirations. The clinician must be wary of more subtle presentations. Several diagnostic tools (TEE, Doppler, CT) can detect intracardiac and cerebral air, but they may not be necessary to confirm the diagnosis of SAE. Cessation of SAE is essential for successful resuscitation. In those with unilateral lung injury, this can theoretically be achieved by isolating and ventilating the noninjured lung. Sole reliance on immediate thoracotomy for hilar clamping to stem the flow of gas emboli is a concept that needs to be challenged. Whether airway and ventilation interventions will eliminate, delay, or decrease the need for thoracotomy and improve the prognosis of SAE remains to be seen. There is little reported in the literature regarding such interventions. Airway management of a patient at risk for SAE should include a technique that can selectively ventilate each lung. Patients with bilateral sources of SAE may benefit from the avoidance of high airway pressures. Regional anesthesia should be considered when appropriate. HBOT is useful in managing cerebral air embolism and should be incorporated as soon as possible. Clinicians involved in trauma care must be familiar with SAE. By adopting a problem-based solution through innovative airway and ventilation management, anesthesiologists may significantly alter and improve the morbidity and mortality rate of SAE resulting from chest trauma.

0 comments Cited 25 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (nlm-ta): J Korean Med Sci

Journal ID (publisher-id): JKMS

Title: Journal of Korean Medical Science

Publisher: The Korean Academy of Medical Sciences

ISSN (Print): 1011-8934

ISSN (Electronic): 1598-6357

Publication date (Print): October 2008

Publication date (Electronic): 30 October 2008

Volume: 23

Issue: 5

Pages: 753-761

Affiliations

[* ]Department of Anesthesiology and Pain Medicine, Anesthesia and Pain Research Institute, Yonsei, University College of Medicine, Seoul, Korea.

[† ]Department of Anesthesia and Perioperative Care, University of California, San Francisco, USA.

[‡ ]Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Seoul, Korea.

Author notes

Address for correspondence: Ki Jun Kim, M.D. Department of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, CPO Box 8044, Seoul 120-752, Korea. Tel: +82.2-2227-3841, Fax: +82.2-312-7158, kkj6063@ 123456yuhs.ac

Article

DOI: 10.3346/jkms.2008.23.5.753

PMC ID: 2580000

PubMed ID: 8955777

SO-VID: 9a4e5556-361e-412b-bb42-dbe023bb767b

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Venous Air Embolism during Surgery, Especially Cesarean Delivery

Read this article at

Abstract

Related collections

RNA drug delivery

Most cited references 86

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

The pathophysiology of failure in acute right ventricular hypertension: hemodynamic and biochemical correlations.

Systemic air embolism after lung trauma.

Author and article information

Journal

Affiliations

Author notes

Article

History

Categories

Comments

Comment on this article

Similar content 586

Most referenced authors 407