Cerebral gas embolism

Douglas J Lanska MD FAAN MS MSPH (Dr. Lanska of the Great Lakes VA Healthcare System and the University of Wisconsin School of Medicine and Public Health has no relevant financial relationships to disclose.)
Originally released October 22, 2003; last updated February 9, 2017; expires February 9, 2020

This article includes discussion of cerebral gas embolism, arterial air embolism, and venous air embolism. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

In this article, the author explains the clinical presentation and pathophysiology of cerebral gas emboli. Cerebral gas emboli may originate from venous or arterial circulations, and the causes, pathophysiology, clinical manifestations, and prognosis differ depending on the circumstances. Iatrogenic instances from diagnostic and chest procedures were reported during the late 1800s and early 1900s, but the frequency of recognized traumatic and iatrogenic cerebral gas embolism increased dramatically after the 1970s. Iatrogenic gas embolism is associated with high mortality: 1 in 5 is dead at 1 year following the event. Independent predictors of mortality at 1 year include cardiac arrest at the time of the accidental gas embolism and admission to an intensive care unit (ICU). Among ICU survivors, independent predictors of survival at 1 year include age, Babinski sign, and acute renal failure.

Key points

 

• Neurologic manifestations are much more common with arterial than venous air emboli, and onset is immediate in the majority. With arterial air emboli, less than 1 cubic centimeter of injected air is sufficient to cause significant central nervous system or cardiac damage or even death.

 

• Findings may include a change in sensorium including coma; seizures or status epilepticus; focal motor (eg, hemiparesis), sensory (eg, paresthesias), or visual findings (eg, visual field deficits); dizziness; or headache. Motor focal findings are by far the most common and the most readily recognized focal neurologic manifestations of air emboli.

 

• Neurologic manifestations of venous air emboli may occur due to cardiovascular compromise or paradoxical embolism via a right-to-left cardiac shunt, pulmonary arteriovenous fistulas, or “overloading” of pulmonary filtering capacities.

 

• Air emboli are usually diagnosed clinically, rather than with diagnostic testing. Although various imaging modalities may show evidence of air or gas emboli, they may also be entirely normal in the face of severe neurologic compromise.

 

• Initially following cerebral gas embolism, 100% oxygen should be administered, with institution of hyperbaric oxygen as soon as possible. Clinical results can be dramatic with hyperbaric oxygen therapy especially if instituted early, but clinically evident benefits have been demonstrated in individual cases even if institution of hyperbaric oxygen therapy was delayed for several hours or even 1 to 2 days.

 

• Iatrogenic gas embolism is associated with high mortality: 1 in 5 is dead at 1 year following the event. Independent predictors of mortality at 1 year include cardiac arrest at the time of the accidental gas embolism and admission to an intensive care unit (ICU). Among ICU survivors, independent predictors of survival at 1 year include age, Babinski sign, and acute renal failure.

 

• Independent predictors of long-term sequelae include focal motor deficit and Babinski sign on ICU admission and duration of mechanical ventilation of at least 5 days.

Historical note and terminology

Human arterial air embolism was recognized as early as 1769 by Italian anatomist Giovanni Battista Morgagni (1682 to 1771), and experimental work on dogs was performed in 1878 by French zoologist and physiologist Paul Bert (1833 to 1886) (Peirce 1980).

Image: Italian anatomist Giovani Battista Morgagni (1761)
Image: French zoologist and physiologist Paul Bert (c1870)
Iatrogenic instances from diagnostic and chest procedures were reported in the late 1800s and early 1900s (Schlaepfer 1922; Peirce 1980), but the frequency of recognized traumatic and iatrogenic cerebral gas embolism increased dramatically after the 1970s in large part due to the advent of computed tomography and magnetic resonance imaging (Ho and Ling 1999).

Cerebral air emboli may originate from venous or arterial circulations, and the causes, pathophysiology, clinical manifestations, and prognosis differ depending on the circumstances. Other types of cerebral gas emboli are also possible but are generally rare and occur under unusual circumstances, such as inhalation of high-pressure helium from unregulated pressurized cylinders (Pao and Hayden 1996; Mitchell et al 2000; Tretjak et al 2002) or laparoscopic use of carbon dioxide (Schindler et al 1995).

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