KEY-WORDS: Venous air embolism

INTRODUCTION
CLINICAL
WORKUP
TREATMENT
FOLLOW-UP
MISCELLANEOUS
BIBLIOGRAPHY

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INTRODUCTION

Background: Venous air embolism (VAE) is the entry of air into the venous system, as a consequence of trauma or iatrogenic complications (especially central venous cannulation or pressurized intravenous infusion systems). It can also occur following various surgical procedures. VAE results in right ventricular dysfunction and pulmonary injury.

Pathophysiology: Entry of air into the venous system produces signs and symptoms through its effects on the right ventricle, the pulmonary circulation or the systemic circulation (if right-to-left shunts are present). Small amounts of air do not produce symptoms as the air is removed from the circulation. Large boluses of air (3.0-8.0 mL/kg) can cause acute right ventricular outflow obstruction and result in cardiogenic shock and circulatory arrest. Intermediate amounts of air end up in the pulmonary circulation and produce a pulmonary vascular injury manifested by pre- and post-capillary pulmonary vasoconstriction, pulmonary hypertension, endothelial injury and permeability pulmonary edema.

The pathogenesis of the pulmonary endothelial injury may have components of platelet-fibrin thrombi from the right ventricle, cytokine release, neutrophil, platelet and complement activation at the microvascular air-blood interface and injury mediated by lipid peroxidation and oxygen radicals.

Frequency:

Mortality/Morbidity: VAE is associated with significant morbidity and mortality. Symptomatic VAE following central venous catheterization has mortality as high as 30%.

• Open chest trauma, blunt chest or abdominal trauma and neck or craniofacial injury are injuries associated with VAE, which may be seen in the ED. Underlying injuries may mask the symptoms of VAE, so an index of suspicion should be maintained.
• The most common ED procedures resulting in VAE are central venous (internal jugular or subclavian) catheterization and pressure infusion of fluids and blood.
• Accidents at home during the use and care of long-term central catheters (e.g., Broviac, Hickman, Port-A-Cath) can lead to VAE.
• Rare cases involving orogenital sex during pregnancy and hydrogen peroxide ingestion have been reported.
• VAE as a complication of orthopedic, neurosurgical and cardiovascular procedures will not typically present to the ED.
• It has been identified as a component of decompression injury as well.

• Symptoms, which develop immediately following embolization, are similar to pulmonary thromboembolism and include:

• Dyspnea
• Chest pain

• Tachycardia

• Hypotension

• Altered sensorium

• The severity of the above symptoms is related to the degree of air entry. Severe cases will present in circulatory shock or sudden death.

Physical:

• Acute respiratory distress

• Tachypnea

• Tachycardia

• Agitation

• Disorientation

• The classic finding on auscultation of the heart is the mill wheel murmur.

• Cyanosis and hypotension accompany severe cases.

Causes:

• VAE results when a pressure gradient develops between a source of air and the venous system, which favors ingress of air into the venous system.

• This may result from a positive pressure on the extravascular side, such as blunt thoracic trauma or air in a rapid fluid infusion system.

• Alternatively, it may result from a negative intravascular pressure, such as occurs during inspiration during central venous catheterization.

• In either case, a communication must exist with the venous system, either traumatic or procedurally (as in central venous catheterization).

• Prevention of VAE during ED procedures is critical. During central venous catheterization, the Trendelenburg position has been traditionally advocated to increase central venous pressure. In spite of this, the risk is present.

• Hyperventilation and agitation increase the risk.

• The use of a closed catheterization system (e.g., Arrow Raulerson syringe) can greatly reduce the risk.

• Vigilance to avoid opening the catheter during subsequent manipulation must be constantly maintained.

• VAE can also occur following catheter removal and may be delayed for 30 min or more; the initial dressing after removal should be occlusive.
  
• Particular care should be undertaken in patients with known right-to-left shunts since paradoxical embolism to the arterial system can occur.

• Arterial blood gases are indicated and usually demonstrate hypoxemia, hypercapnia and metabolic acidosis. Mild cases may demonstrate mild hypoxemia and hypocapnia.

• Other laboratory studies are non-specific and are obtained as indicated by associated conditions.

Imaging Studies:

• Chest x-ray:

• The x-ray may be normal or may reveal air in the pulmonary arterial system.

• Other radiographic signs which may be present include pulmonary arterial dilatation, focal oligemia (Westermark's sign) and pulmonary edema.

• Transthoracic or transesophageal echocardiography can assist in establishing the presence of air in the right ventricular outflow tract or major pulmonary veins. Simple precordial Doppler may allow rapid detection.

Other Tests:

• Electrocardiographic (ECG) findings, if present, are the same as those found in venous thromboembolism:

• Tachycardia

• Right axis deviation

• Right ventricular strain

• ST depression

• An increased dead space may be present and can be identified as an increased end-tidal to arterial blood carbon dioxide gradient (normal less than 5.0).

Procedures:

• If a central venous catheter is in place, measure the central venous pressure. It is usually elevated in symptomatic VAE.
  
• Aspiration of air from a central venous catheter may help establish the diagnosis.

• Once suspected, any central line procedure in progress is immediately terminated and the line is clamped.
• Do not withdraw the catheter at this time unless it cannot be clamped.
• The patient is promptly placed in the Trendelenburg position and rotated toward the left lateral decubitus position.
• This maneuver will help trap air in the apex of the ventricle and prevent its ejection into the pulmonary arterial system, as well as maintain right ventricular output.

• Administer 100% oxygen and intubate for significant respiratory distress or refractory hypoxemia.

• If a central venous catheter is present, aspirate from the distal port and attempt to remove air. The catheter may have to be advanced for this to be successful.

• In cases of circulatory collapse, external cardiac compression may help to expel air from the pulmonary outflow tract and disperse it into the peripheral pulmonary venous system. Support right ventricular function with fluid administration and beta-adrenergic agents if indicated.

• Experience with hyperbaric oxygen therapy for VAE is limited, but experience suggests significant efficacy. If this modality is available, arrange transportation to a hyperbaric facility without delay.

• Hyperbaric medicine for symptomatic venous air embolism syndrome

• Patients should be admitted to the ICU. Pulmonary insufficiency may develop following VAE.
  
  

• Failure to recognize early signs of VAE following central venous procedures

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