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Venous Air Embolism Treatment & Management

  • Author: Brenda L Natal, MD, MPH; Chief Editor: Erik D Schraga, MD  more...
 
Updated: Dec 08, 2015
 

Emergency Department Care

If VAE is known about prior to presentation to the emergency department (ED), affected patients should be transported in the left lateral decubitus position.[7]

Management of venous air embolism (VAE), once is suspected, includes identification of the source of air, prevention of further air entry (by clamping or disconnecting the circuit), a reduction in the volume of air entrained, and hemodynamic support. 

Note the following

  • Administer 100% O2 and perform endotracheal intubation for severe respiratory distress or refractory hypoxemia or in a somnolent or comatose patient in order to maintain adequate oxygenation and ventilation. Institution of high flow (100%) O2 will help reduce the bubble's nitrogen content and therefore size.[1, 4, 7, 8, 9, 11, 19, 26]
  • Immediately place the patient in the left lateral decubitus (Durant maneuver) and Trendelenburg position. This helps to prevent air from traveling through the right side of the heart into the pulmonary arteries, leading to right ventricular outflow obstruction (air lock). If CPR is required, place the patient in a supine and head-down position.[1, 7, 9, 11, 19]
  • Direct removal of air from the venous circulation by aspiration from a central venous catheter in the right atrium may be attempted. However, no current data support emergent catheter placement for air aspiration during an acute setting of VAE-induced hemodynamic instability.[1, 4, 9, 11]
  • If necessary, initiate cardiopulmonary resuscitation (CPR). Other than maintaining cardiac output, CPR may also serve to break large air bubbles into smaller ones and force air out of the right ventricle into the pulmonary vessels, thus improving CO. Even without the need for CPR, this rationale holds for closed-chest massage. Animal studies have shown that the benefit of cardiac massage equals that of left lateral recumbency, as well as intracardiac aspiration of air.[1, 4, 9, 11]
  • Admit patients to the intensive care unit (ICU), as they may develop cardiopulmonary distress/failure following VAE.
  • Consider transfer to a hyperbaric oxygen therapy (HBOT) facility. Indications for HBOT include neurological manifestations and cardiovascular instability. Potential benefits include compression of existing bubbles, establishing a high diffusion gradient to speed resolution of existing bubbles, improved oxygenation of ischemic tissues, and lowered intracranial pressure. Immediate HBOT, once venous air embolism (VAE) is diagnosed, is recommended; however, prognosis may still be good if therapy is initiated beyond 6 hours of event. Prompt transfer to an HBOT center has been reported to decrease the mortality rate in patients with cerebral air embolism. If transfer is necessary, ground transportation is preferred. If air transportation cannot be avoided, the lowest altitude should be sought.[1, 4, 7, 9, 10, 11, 14, 38]
  • Supportive therapy should include fluid resuscitation (to increase intravascular volume, increase venous pressure and venous return). Also some evidence exists that gas emboli may cause a relative hemoconcentration, which increases viscosity and impairs the already compromised circulation. Hypovolemia is less tolerated than relative anemia. In animal studies, moderate hemodilution to a hematocrit of 30% reduces neurologic damage. Crystalloids may cause cerebral edema; therefore, colloids are preferred for hemodilution.[1, 4, 14]
  • The administration of vasopressors and mechanical ventilation are two other supportive measures that may necessary.[1, 4, 37] In a case report of a patient undergoing a craniotomy who showed cardiopulmonary findings suggestive of acute venous air embolism, inotropic treatment with ephedrine seemed to rapidly reverse the cardiopulmonary abnormalities. Early inotropic support of the right ventricle has been recommended if venous air embolism is suspected.[37]
  • In animal studies, the use of perfluorocarbons (FP-43) has been shown to enhance the reabsorption of bubbles and the solubility of gases, thereby decreasing both the neurologic and cardiovascular complications of systemic and coronary venous air embolism. These benefits, however, have not been validated in humans.[1]
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Prevention

The optimal management of venous air embolism (VAE) is prevention. Minimizing the pressure gradient between the site of potential entry and the right atrium is essential in prevention of VAE.

Potential measures to reduce the risk and/or severity of VAE during neurosurgical interventions include the following[34] :

  • Using a modified semi-sitting or lounging position for the patient, in which the head is lower than the legs to create a positive pressure in the transverse and sigmoid sinuses
  • Avoiding hyperventilation in the sitting position
  • Using a sitting position, under strict protocol, for procedures in patients with known patent foramen ovale 

Measures to reduce the risk of air embolism during mechanical ventilation and central line insertion/removal/manipulation should be taken. With regard to these two procedures, the following interventions should be implemented:

  • Prevent barotraumas by minimizing airway pressures during mechanical ventilation.
  • Avoid PEEP as it impairs hemodynamic performance, does not protect against air embolism, and probably increases risk of paradoxical emboli.
  • Avoid and treat hypovolemia prior to catheter placement.
  • Occlude the needle hub during catheter insertion/removal.
  • Maintain all connections to the central line closed/locked when not in used (use Luer-lock syringes for blood draws from catheters).
  • During catheter insertion/removal, place the patient in the supine position with head lowered (insertion site should be 5 cm below right atrium). If the patient is awake he or she may assist by holding his or her breath or by doing a Valsalva maneuver, both of which can increase the central venous pressure
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Contributor Information and Disclosures
Author

Brenda L Natal, MD, MPH Assistant Professor of Emergency Medicine, Simulation Director, Rutgers New Jersey Medical School; Attending Physician, Department of Emergency Medicine, University Hospital of Newark

Brenda L Natal, MD, MPH is a member of the following medical societies: American College of Emergency Physicians, American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Christopher I Doty, MD, FAAEM, FACEP Associate Professor of Emergency Medicine, Residency Program Director, Vice-Chair for Education, Department of Emergency Medicine, University of Kentucky-Chandler Medical Center

Christopher I Doty, MD, FAAEM, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

David Eitel, MD, MBA Associate Professor, Department of Emergency Medicine, York Hospital; Physician Advisor for Case Management, Wellspan Health System, York

David Eitel, MD, MBA is a member of the following medical societies: American College of Emergency Physicians, American Society of Pediatric Nephrology, Society for Academic Emergency Medicine, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Additional Contributors

Daniel J Dire, MD, FACEP, FAAP, FAAEM Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Pediatrics, American Academy of Emergency Medicine, American College of Emergency Physicians, Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous authors, Andrew G Wittenberg, MD, MPH; Allison J Richard, MD; and Steven A Conrad, MD, PhD, to the development and writing of this article.

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