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Venous Air Embolism Clinical Presentation

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

History

Most venous air emboli go unrecognized because their presentations are protean and mimic other cardiac, pulmonary, and neurologic dysfunctions, such as the following (in awake patients)[12, 25] :

  • Acute dyspnea, tachypnea
  • Continuous cough
  • "Gasp" reflex (a classic gasp at times reported when a bolus of air enters the pulmonary circulation and causes acute hypoxemia) [1, 2]
  • Dizziness/lightheadedness/vertigo
  • Nausea
  • Headache, seizures
  • Syncope
  • Substernal chest pain
  • Slurred speech
  • Blurred vision
  • Anxiety/agitation/disorientation/sense of "impeding doom"
  • Ataxia

 

Because of the lack of specific signs and symptoms of venous air embolism (VAE), a high index of suspicion is necessary to establish the diagnosis and institute the appropriate treatment. The number of procedures that place patients at risk for VAE has increased, and these procedures occur across almost all clinical specialties. This must be considered to aid in the confirmation or ruling out of VAE.

If VAE is suspected, obtain the following key historical elements:

  • Recent surgical procedures especially neurosurgical, otolaryngological, cardiovascular, or orthopedic
  • Scuba diving trips and a history of decompression injuries or decompression sickness
  • Blunt or penetrating trauma to the head, face, neck, thorax, and/or abdomen
  • Invasive therapeutic and/or diagnostic procedures such as central venous catheterization; lumbar puncture; high-pressure infusion of medications, blood products, and/or IV contrast agents
  • Patients with hemodialysis access catheters or other indwelling central venous catheters
  • Patients on positive pressure ventilation
  • Peripartum/postpartum orogenital sex (air may enter veins of the myometrium) [4, 7]
  • Ingestion of hydrogen peroxide (rare)
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Physical Examination

Clinical Presentation

Many cases of venous air embolism (VAE) are subclinical and do not result in untoward outcomes. However, severe cases are characterized by cardiovascular collapse and/or acute vascular insufficiency of several specific organs, including, but not limited to, the brain, spinal cord, heart, and skin. As mentioned earlier, the spectrum of effects is largely dependent on the rate and volume of entrained VAE.[1, 6, 11]

Two additional contributing factors include whether or not the patient is spontaneously breathing (yielding negative thoracic pressure) or is under controlled positive pressure ventilation.[1]  These two factors facilitate the entry of air down a pressure gradient. The clinical presentation is also dependent on the patient's body position at the time of the event. Generally, if the patient is in a sitting position, gas will travel retrograde via the internal jugular vein to the cerebral circulation, leading to neurologic symptoms secondary to increased intracranial pressure. In a recumbent position, gas proceeds into the right ventricle and pulmonary circulation, subsequently causing pulmonary hypertension and systemic hypotension.[11]

An arterial air embolism can also form if passage of air occurred through a right-to-left shunt, as in the case of a patent foramen ovale.[2, 3]  The arterial air emboli can then lodge in the coronary or cerebral circulation, causing myocardial infarction or stroke.

Signs

The following hemodynamic, pulmonary, and neurologic complications primarily result from gas gaining entry into the systemic circulation, occluding the microcirculation and causing ischemic damage to these end organs. Animal studies have also suggested the presence of secondary tissue damage resulting from the release of inflammatory mediators and oxygen free radicals that occur in response to air embolism.

Cardiovascular signs include the following

  • Dysrhythmias (tachyarrhythmias/bradycardias)
  • "Mill wheel" murmur - A temporary loud, machinerylike, churning sound due to blood mixing with air in the right ventricle, best heard over the precordium (a late sign) [2, 9, 11]
  • JVD
  • Hypotension
  • Myocardial ischemia
  • Nonspecific ST-segment and T-wave changes and/or evidence of right heart strain [1, 2, 33]
  • Pulmonary artery hypertension
  • Increased CVP
  • Circulatory shock/cardiovascular collapse

Pulmonary features include the following:

  • Adventitious sounds (rales, wheezing)
  • Tachypnea
  • Hemoptysis
  • Cyanosis
  • Decreased end-tidal carbon dioxide, arterial oxygen saturation, and tension
  • Hypercapnia
  • Increased pulmonary vascular resistance and airway pressures
  • Pulmonary edema
  • Apnea

Neurologic findings include the following:

  • Acute altered mental status
  • Seizures
  • Transient/permanent focal deficits (weakness, paresthesias, paralysis of extremities)
  • Loss of consciousness, collapse
  • Coma (secondary to cerebral edema)

Funduscopic examination may reveal ophthalmologic signs such as air bubbles in the retinal vessels.[14]

Dermatologic evaluation may reveal crepitus over superficial vessels (rarely seen in setting of massive air embolus) and/or livedo reticularis.

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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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