Other Embolic Syndromes

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63 Other Embolic Syndromes

The presentation, pathophysiology, and treatment of embolic disease other than thromboembolic processes are discussed in this chapter. Included are emboli associated with iatrogenic complications of medical diagnostic and therapeutic manipulations as well as sequelae from skeletal trauma and pregnancy.

image Air Embolism

Air embolism, the entry of gas into the vasculature, is a largely iatrogenic clinical entity that can result in serious morbidity and even mortality (Table 63-1).1 This is one of the most serious problems in diving medicine.2 The medical use of a variety of gases has created numerous types of gas embolisms, including carbon dioxide, nitrous oxide, and nitrogen emboli. There are two broad categories of gas embolism, venous and arterial, depending on the mechanism of gas entry and where the emboli ultimately lodge.

TABLE 63-1 Medical Specialties with Documented Cases of Gas Embolism

Specialty Mechanism of Gas Embolism
All medical specialties Inadvertent entry of air through peripheral intravenous circuits
All surgical specialties Intraoperative use of hydrogen peroxide, generating arterial and venous oxygen emboli
Anesthesiology Entry of air through disconnected intravascular catheters, inadvertent infusion of air through intravascular catheters
Cardiac surgery Entry of air into extracorporeal bypass pump circuit, incomplete removal of air from the heart after cardioplegic arrest, carbon dioxide–assisted harvesting of peripheral veins
Cardiology Entry of air through intravascular catheters during angiographic studies and procedures
Critical care/pulmonology Entry of air through disconnected intravascular catheters, pulmonary barotrauma, rupture of intraaortic balloon pumps, entry of air in extracorporeal membrane oxygenator (ECMO) circuit
Diving medicine and hyperbaric medicine Pulmonary barotrauma, paradoxical embolism after decompression injury, entry of gas through disconnected intravascular catheters
Endoscopic/laparoscopic surgery Entry of gas into veins or arteries during insufflation of body cavities
Gastroenterology Entry of gas into veins during upper and lower endoscopies and endoscopic retrograde pancreatography (ERCP)
Neonatology/pediatrics Pulmonary barotrauma in treatment of infants with premature lungs
Nephrology Inadvertent entry of air through hemodialysis catheters and circuits on hemodialysis machine
Neurosurgery Entry of air through incised veins and calvarial bone, especially during sitting craniotomies
Obstetrics/gynecology Cesarean sections, gas insufflation into veins during endoscopic surgery, intravaginal/intrauterine gas insufflation during pregnancy
Otolaryngology Laser (Nd:YAG) surgery on the larynx and trachea/bronchi
Orthopedics Gas insufflation into veins during arthroscopy, total hip arthroplasty, prone spine surgery
Radiology Injected air/gas as contrast agent, inadvertent injection of air during angiographic studies
Thoracic surgery Entry of air into pulmonary vasculature during lung biopsies and video-assisted thoracoscopy (VATS), chest trauma (penetrating and blunt), lung transplants
Urology Transurethral prostatectomy (TURP), radical prostatectomy
Vascular surgery Entry of air during carotid endarterectomies

Venous Gas Embolism

A venous gas embolism occurs as a result of the entry of gas into the systemic venous system.3 The gas is then transported to the lungs via the pulmonary arteries, causing interference in gas exchange, arrhythmias, pulmonary hypertension, right ventricular strain, and cardiac failure. Predispositions that allow entry of gas into the venous system include incision of noncollapsed veins and the presence of subatmospheric pressure in these vessels. These conditions occur when the surgical field is above the level of the heart (for instance, during neurosurgical operations performed in the sitting position).4 Other potential pathways include entry of air into central venous and hemodialysis catheters1 and entry of air into the veins of the myometrium in the peripartum period.1,5


The most common scenario for venous gas embolism is insidious, where there is continuous entry of small gas bubbles into the venous system. With rapid entry or larger volumes of gas, increasing strain on the right ventricle follows because of the migration of the emboli to the pulmonary circulation. Pulmonary arterial pressure increases, while increased resistance to right ventricle outflow causes diminished pulmonary venous return. This is reflected in decreased left ventricular preload, resulting in diminished cardiac output and, ultimately, systemic cardiovascular collapse.6 Quite often, tachyarrhythmias develop, but bradycardias are possible as well. When large quantities of gas/air (over 50 mL) are injected abruptly, acute cor pulmonale and/or asystole can occur.3 These alterations of lung vessel resistance and ventilation/perfusion mismatch in the lung cause intrapulmonary right-to-left shunt with increased alveolar dead space, leading to arterial hypoxia and hypercapnia.


The so-called mill-wheel cardiac murmur, a continuous churning murmur, is relatively typical of venous gas embolism and can be auscultated by a precordial or esophageal stethoscope. A capnometric decrease of end-tidal carbon dioxide suggests ventilation/perfusion mismatching resulting from obstruction of the pulmonary arteries.7 Precordial Doppler ultrasonography is a sensitive and practical monitor to detect intracardiac air,1,8 but an even more sensitive and specific monitor in procedures with a high risk for gas embolism is transesophageal echocardiography (TEE). TEE is the current gold standard for detecting intracardiac gas; however, this technique requires significant training in application and interpretation to be effective.1,9


When a diagnosis of venous gas embolism is considered (Table 63-2), further entry of gas into the venous circulation must be avoided. Catecholamine therapy and cardiopulmonary resuscitation should be initiated for cardiovascular collapse. Adequate oxygenation is often only possible with a significant increase in the oxygen concentration of the inspired gas (i.e., 100% oxygen); 100% oxygen also reduces the size of the gas embolism by increasing the gradient for nitrogen egress from the bubble.10 Rapid-volume resuscitation is recommended to elevate venous pressure, thus decreasing the continued entry of gas into the venous circulation. Some authors recommend attempting to evacuate air from the right ventricle by a central venous catheter (multi-orifice catheters may be more effective than a single lumen) or a pulmonary arterial catheter.11 A left-lateral decubitus position had been recommended in the past but has largely been abandoned because recent hemodynamic studies showed no benefit. Hyperbaric oxygen therapy is not a first-line treatment but may be a useful adjunct in severe cases and should certainly be considered if there are neurologic findings. If central nervous system symptoms are present, a paradoxical embolism should be presumed.

TABLE 63-2 Treatment of Gas Embolism

  Venous Gas Embolism Arterial Gas Embolism
Prevent further gas entry Increase venous pressure (e.g., Valsalva, IV fluids)
Identify and disable entryway for gas
Identify and disable the entryway for gas
Definitive therapy Supportive Hyperbaric oxygen therapy as soon as the patient is stable for transfer to a hyperbaric oxygen facility
Supportive therapy Oxygen, intravascular volume expansion, catecholamines Oxygen, intravascular volume expansion, catecholamines
Positioning Supine Supine
Evacuation of embolized gas Aspiration of multilumen central venous catheter; patient in left lateral decubitus position Hyperbaric oxygen
Adjunctive therapy Hyperbaric oxygen Lidocaine, antiepileptics

Paradoxical Embolism

A paradoxical embolism arises when air/gas entrained in the venous circulation enters the systemic arterial circulation, causing symptoms of end-artery obstruction. There are a number of mechanisms by which this can occur, such as the passage of gas across a patent foramen ovale to the systemic circulation. A patent foramen ovale is detectable in about 30% of the population and makes right-to-left shunting of gas bubbles possible.12 Elevated pulmonary arterial pressure due to a venous gas embolism may be reflected in elevated right atrial pressures predisposing to bubble transport across a patent foramen ovale. In addition, the decrease in left atrial pressure caused by mechanical ventilation and use of positive end-expiratory pressure may create a pressure gradient across the patent foramen ovale favoring passage of gas into the systemic circulation.1

Venous gas may enter the arterial circulation by overwhelming the filtering capacity of the lungs that normally prevents arterial gas emboli. Clinical cases are documented in which a fatal cerebral arterial gas embolism developed as the result of a large venous gas embolism, but no intracardiac defects or shunt mechanisms could be demonstrated.13 The filtration threshold of the pulmonary circulation for gas emboli can be affected by various anesthetic agents. In particular, in experimental studies, volatile anesthetics have been shown to reduce the threshold for spillover of venous bubbles into systemic arteries.14


Therapy of paradoxical embolism is identical to that of a primary arterial gas embolism (see Table 63-2). It should be stressed that every venous gas embolism has the potential to evolve into an arterial gas embolism.

Arterial Gas Embolism

Arterial gas embolism occurs though the entry of gas into the pulmonary veins or directly into the arteries of the systemic circulation. Mechanisms include overexpansion of the lung through decompression barotrauma in diving, pulmonary barotrauma from positive-pressure ventilation in critical care patients, and paradoxical embolism. Additionally, cardiac surgical procedures with extracorporeal bypass are a potential mechanism for these events.1 The entry of even small amounts of gas into the arterial system leads to a flow of gas bubbles into functional end arteries and occlusion of these vessels. Although possible in all arteries, the embolic obstruction of the coronary arteries or the nutritive arteries of the brain, termed cerebral arterial gas embolism, is especially critical and can be fatal owing to the vulnerability of these organs to short periods of hypoxia.


Entry of gas into the aorta causes distribution of gas bubbles into nearly all organs. Small emboli in the vessels of the skeletal muscles or viscera are well tolerated, although organ dysfunction such as rhabdomyolysis and/or renal insufficiency may occur.15 Embolization to the cerebral or coronary circulation may result in severe morbidity or death. Embolization into the coronary arteries can induce electrocardiographic changes typical of ischemia and infarction, with arrhythmias, myocardial depression, cardiac failure, and cardiac arrest. Circulatory responses may also be seen with embolization to the cerebral vessels.16 Cerebral arterial gas embolization typically involves migration of gas to small arteries of the brain. The emboli generate pathology by two broad mechanisms: reduced perfusion distal to the obstruction and an inflammatory response to the bubble.1