Aeroembolism


Aeroembolism

Description, Causes and Risk Factors:

Aeroembolism is an uncommon but potentially catastrophic event which occurs as a consequence of the entry of air into the vasculature. A venous, or pulmonary aeroembolism occurs when air enters the systemic venous circulation and travels to the right ventricle and/or pulmonary circulation. An arterial aeroembolism results from introduction of air into the arterial system and can produce ischemia of any organ with poor collateral circulation.

Two conditions must be present for aeroembolism to occur:

    A direct communication between a source of air and the vasculature must exist.

  • A pressure gradient favoring the passage of air into the circulation (rather than bleeding from the vessel) must be present.

Surgery — Venous aeroembolism most commonly complicates neurosurgical and otolaryngological interventions because the surgical incision is made at a level above the heart by a distance greater than the central venous pressure. This is a particular problem if the patient is placed in the Fowler's, or sitting position, which further increases negative venous pressure relative to the atmosphere. The estimated incidence of venous aeroembolism during neurosurgical procedures ranges from 10 percent (for surgical patients in the prone position) to 80 percent (for patients undergoing repair of cranial synostosis while in the Fowler's position). Most episodes are clinically silent or result in mild, transient hypotension.

Penetrating chest injuries may produce a bronchopulmonary venous fistulae and arterial air emboli. The mortality rate in one series of 9 patients with this complication was 66 percent. Aeroembolism has also been reported following Nd:YAG laser treatment of endobronchial lesions, likely due to coolant gas (which exits the bronchoscope under high flow/high pressure conditions to cool the laser probe) entering the pulmonary venules and gaining access to the systemic circulation.

aeroembolism

Central venous catheterization — Venous aeroembolism is a serious and often under-recognized complication of central venous catheterization. The incidence of line-associated aeroembolism has varied from 1 in 3000 to 1 in 47 in different reports. Venous air emboli can occur at the time of central line or pulmonary artery catheter insertion, while the catheter is in place, or at the time of catheter removal.

Divers are also at risk for aeroembolism, and one series estimated that aeroembolism complicate approximately 7 of every 100,000 dives. Rapid ascent without exhalation can result in expansion of gas in the lungs and consequent alveolar rupture. If pulmonary veins tear as the alveoli rupture, air can return to the left heart with oxygenated blood and can embolize within the arterial system to produce tissue ischemia.

Symptoms:

A number of physiologic changes can ensue, including:

    Hypoxemia, due to alveolar flooding and ventilation-perfusion mismatching.

  • Increased physiologic dead space, with a rise in PaCO2 if ventilation is held constant.

  • Decreased lung compliance secondary to pulmonary edema.

  • Increased airway resistance, postulated to be due to release of bronchoconstricting mediators such as serotonin and histamine from endothelium damaged by the air bubbles.

Systemic complications of aeroembolism — Air bubbles in the microcirculation directly occlude blood flow and cause ischemic damage to end-organs, such as the brain, spinal cord, heart, and skin. Secondary tissue damage from the release of inflammatory mediators and oxygen free radicals in response to aeroembolism has also been suggested by animal experiments.

Diagnosis:

Minor cases of aeroembolism occur frequently and are minimally symptomatic. Severe cases are characterized by hemodynamic collapse and/or acute vascular insufficiency of specific organs such as the brain or spinal cord. Differentiation from pulmonary thromboemboli, acute myocardial infarction, or cerebrovascular accident may be difficult. Dyspnea is an almost universal finding, and may be accompanied by substernal chest pain and a subjective sense of doom.

Aeroembolism should be considered in the differential diagnosis of any patient who has the sudden onset of cardiopulmonary or neurologic decompensation in a clinical setting which puts the patient at risk for aeroembolism.

Confirming the diagnosis of aeroembolism is difficult and is complicated by the fact that air may be rapidly absorbed from the circulation while diagnostic tests are being arranged. Exclusion of other life-threatening processes is generally required.

Some of the following techniques may be useful in supporting the clinical diagnosis of aeroembolism:

    Laboratory, hemodynamic, and chest x-ray findings — One study documented significant elevations in serum creatine kinase activity in all of 22 divers with arterial aeroembolism, but not in 22 control divers. The sensitivity of elevated serum creatine kinase activity in other populations with arterial aeroembolism has not been reported.

  • Echocardiography — Transthoracic and transesophageal echocardiography have been used to document the presence of air in the right ventricle and may show evidence of acute right ventricular dilation and pulmonary artery hypertension consistent with aeroembolism. Continuous monitoring with echocardiography or transcranial Doppler techniques have been used during high-risk surgical procedures to detect aeroembolism in the preclinical phase.

  • End-tidal CO2 monitoring — The worsening of ventilation-perfusion matching and increase in physiologic dead space which occur with venous aeroembolism produce a fall in end-tidal CO2 and may raise intraoperative suspicion of the condition. However, this finding is nonspecific and also occurs with pulmonary embolism, massive blood loss, circulatory arrest, or disconnection from the anesthesia circuit. The combination of intraoperative echocardiography and end-tidal CO2 monitoring may increase intraoperative sensitivity in detecting preclinical air emboli in high-risk patients.

  • Pulmonary artery catheters — A rise in pulmonary artery pressure may be observed when venous aeroembolism occurs in a patient in whom a pulmonary artery catheter has been placed. However, this is a nonspecific finding, with an estimated sensitivity of only 45 percent.

  • Ventilation-perfusion scan — Ventilation-perfusion scan abnormalities which mimic those seen in pulmonary thromboembolism may be seen in the setting of massive aeroembolism. However, the perfusion defects due to aeroembolism resolve more rapidly, frequently within 24 hours.

  • Chest CT — Chest CT may detect air emboli in the central venous system (especially the axillary and subclavian veins), right ventricle, or pulmonary artery. The specificity of these findings is greatest when large defects are detected because small (<1 mL), asymptomatic air emboli occur during the performance of 10 to 25 percent of contrast-enhanced CT scans if carefully sought. False positive studies may be more common when higher resolution or electron beam CT scanners are used.

  • Pulmonary angiography — Pulmonary angiography may be normal in patients who have suffered aeroembolism because of rapid resorption of air between the time of presentation and the performance of the procedure. If positive, vascular occlusion and/or findings consistent with vasoconstriction may be seen, including "corkscrewing" of vessels, tapering of vessels, and delayed emptying of vessels in the affected versus the unaffected lung.

Treatment:

The primary aims of treatment are identification of the source of air entry and prevention of further air embolization, removal of embolized gas, and restoration of the circulation. Supportive care (eg, the use of mechanical ventilation, vasopressors, volume resuscitation as indicated) is the cornerstone of management, but several active measures may also be helpful.

Nitrogen washout — High-flow supplemental oxygen increases the partial pressure of oxygen and decreases the partial pressure of nitrogen in blood. This produces a positive pressure gradient for the diffusion of nitrogen from the air bubbles to the blood, accelerating bubble resorption. In contrast, nitrous oxide, when given during general anesthesia, can diffuse from blood to air emboli, causing clinical deterioration as gas bubbles enlarge. Thus, nitrous oxide (N2O) should be discontinued at the first suspicion of aeroembolism.

Hyperbaric therapy — Patients with continued evidence of cardiopulmonary compromise or neurologic deficits generally should receive treatment with hyperbaric oxygen therapy (HBO). HBO reduces air bubble size, accelerates nitrogen resorption, and increases the oxygen content of arterial blood, potentially ameliorating ischemia. Although prompt initiation of HBO is preferred, it may improve outcome even if delayed up to 30 hours. No randomized controlled trials of HBO in aeroembolism have been conducted in humans, and the potential benefits of HBO must be weighed against the potential risks of transport to the HBO facility.

Patient positioning — Patients who develop an "air lock" from a large gas bubble obstructing the right ventricular outflow tract may benefit from maneuvers which float air emboli into other areas of the ventricle. Both the left lateral decubitus position (Durant's maneuver) and the Trendelenburg position can restore forward blood flow by placing the right ventricular outflow tract inferior to the right ventricular cavity, permitting air to migrate superiorly to a non-obstructing position.

Closed-chest cardiac massage — Closed-chest cardiac massage forces air out of the pulmonary outflow tract into smaller pulmonary vessels, thus improving forward blood flow. This technique improved survival in dogs as effectively as positioning and intracardiac aspiration of air.

Aspiration of air from the venous circulation — Air has been successfully aspirated from the right ventricle via a percutaneously introduced needle or a central venous catheter in several experimental models and case reports. In general, however, these maneuvers are of limited benefit because the volume of air recovered is less than 20 mL. Most authors recommend attempting to aspirate air only if a central venous catheter is already in place.

NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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