Venous Gas Embolism

Etiology

Venous gas embolisms are usually caused by medical interventions that expose the venous circulation to outside air or gas. Examples of procedures and situations that have caused venous gas embolisms include central venous catheter insertion/removal, CT injector, hemodialysis, penetrating chest injuries, lung biopsy, cardiovascular surgery, neurosurgery, angioplasty, arthroscopy, laparoscopic procedures, and hysteroscopy, among many others.

Anytime the patient is with the head elevated or Fowler position, air embolism is a risk during surgery. Air embolism has been reported after ENT procedures and neurosurgery. Both gynecologic and obstetric procedures have the potential to cause venous air embolism. The risk of air embolism is highest when the uterus is exteriorized during a cesarean section. A common cause of venous air embolism is central venous access. This may be due to failure to occlude the needle hub, detachment of the catheter connections, deep inspiration during the line's removal or insertion, the patient's upright position during insertion, and hypovolemia.

Another common cause of venous air embolism is mechanical insufflation during hysteroscopy, laparoscopy, or during a urethral procedure. Finally, positive pressure ventilation also places the patient at risk of venous gas embolism. Overdistension and rupture of the alveoli with high PEEP can lead to free air.

The common factor in these procedures is the possibility of introducing air/gas into the venous circulation. Additionally, deep-sea diving can result in nitrogen gas coalescing in the venous system as the diver ascends. When ascending, the pressure decreases, and the nitrogen dissolved in the blood at a much higher temperature forms bubbles and is no longer kept in solution with the blood. The nitrogen boils out of the venous system, particularly as this is a lower-pressure system. The nitrogen gas forms bubbles and coalesce into emboli. This is prevented by slowly ascending and ensuring the diver has adequate breaths as they ascend to wash out excess nitrogen via exhalation.[1][2][3][4][5]

Epidemiology

Due to an increase in invasive medical procedures, the incidence of gas embolism has been steadily increasing. Additionally, the use of end-tidal carbon dioxide and Doppler monitoring has led to an increase in gas embolus detection. However, the actual incidence is unknown because most venous gas emboli are largely subclinical and do not result in any obvious symptoms in patients. Neurosurgical procedures have the highest risk of a venous gas embolus due to the patient being upright, the position of the brain relative to the heart, and the brain's noncompressed venous system.

Pathophysiology

The severity of venous gas embolism depends on the rate of gas introduced into circulation, the volume of gas, and the patient's position. Rapid gas entry and larger volumes of gas increase the size of the venous gas embolism and the severity of symptoms. Assuming no right-to-left shunting occurs, the venous gas embolus lodges in the pulmonary artery in the lungs. This can cause pulmonary artery hypertension and subsequent right heart strain. Occasionally, the gas embolus can pass through the pulmonary artery and make its way to the left heart and into the systemic arterial circulation, possibly causing far more severe sequelae such as stroke. This can also happen with right-to-left shunts such as a fistulous tract or a patent foramen ovale, allowing the embolus to travel to the systemic arterial circulation, thus bypassing the lungs. This is called an arterial gas embolus or paradoxical embolism.[6][7]

In most cases, small amounts of air are broken down in the capillary bed and absorbed into the systemic circulation without any sequelae. It is estimated that more than 5 ml/kg of air must be introduced into the venous system to produce symptoms. However, complications can occur with even 20 ml of air. Sometimes, even injection of 1 to 2 ml of air into the CNS can be fatal. Further, as little as 0.5 ml of air introduced into the coronary arteries can initiate ventricular fibrillation. The closer the air is injected into the right heart, the higher the risk of complications.

Large amounts of air introduced into the right ventricle can obstruct the outflow tract, especially if the pulmonary artery pressures are high. When venous air embolism occurs, both tachy and bradyarrhythmias can occur. In patients with a right-to-left shunt (e.g., VSD, ASD, PFO), venous air embolism can prove to be even more dangerous, as the air can enter the arterial system and induce a stroke, mesenteric ischemia, or death.

History and Physical

A history of recent surgical procedures or trauma increases the suspicion of venous gas embolism. It can sometimes be difficult to diagnose due to the similarity to other causes of the patient's symptoms. Clinical manifestations of venous gas embolism include the following: Right heart strain on EKG, tachyarrhythmias, hypotension, dyspnea, chest pain, and coughing. If the patient is being monitored, a decrease in end-tidal CO2 and hypercapnia may be seen. Increased pulmonary artery pressure may also be seen if invasive monitoring is established. If severe hypotension due to pulmonary artery hypertension and right heart strain is present, an altered mental status may also be seen. Arterial gas emboli are not discussed here but can lead to stroke and myocardial infarction, among other sequelae.

Cardiac signs of venous air embolism include:

• A mill-wheel murmur, which is loud and machinery-like
• Tachy or bradyarrhythmias
• Elevation in jugular venous pressure
• Hypotension
• Myocardial ischemia

Pulmonary features include:

• Tachypnea
• Rales, wheezing
• Cyanosis
• Mild hemoptysis
• Apnea

CNS features include:

• Altered mental status
• Seizures
• Coma
• Transient focal neurological deficits

An eye examination may reveal air bubbles in the retinal vessels. With massive air embolism, skin palpation may reveal crepitus over the superficial veins. Because there are no specific signs and symptoms, a high index of suspicion is required to make the diagnosis and initiate treatment.

Evaluation

The diagnosis of venous gas embolism is largely clinical and requires high suspicion. Sudden symptoms after or during an invasive procedure, such as loss of consciousness or hemodynamic instability, are highly suggestive of gas embolism. The temporal relationship between symptoms and invasive procedures is the biggest clue in making the diagnosis. Various monitors used during surgery that may already be in place can help diagnose venous gas embolism or arterial gas embolism. The blood gas may reveal hypercapnia, hypoxemia, and metabolic acidosis. Transesophageal echocardiography may visualize a gas bubble in the heart and is the most sensitive diagnostic test for venous gas emboli. Precordial Doppler monitoring is the most sensitive, noninvasive test routinely used. As noted, end-tidal carbon dioxide and nitrogen monitoring are useful in detecting venous gas emboli lodged into the pulmonary vasculature. Additionally, a drop in tidal volume is more specific for venous gas embolism than many other tests.

CT scans can detect small amounts of air in the central venous system. The technique may also reveal intracerebral air or cerebral edema. End-tidal nitrogen is a very sensitive method of detecting venous air embolism. The response is much faster than with ETC02 measurements. However, the technique does not always identify minute amounts of air and may falsely indicate resolution. If the patient has a central venous catheter, aspiration may reveal the presence of air bubbles. Anytime venous air embolism is suspected, the surgical procedure must be quickly terminated. Aspiration may occur when inserting a central venous catheter. The catheter should ideally be placed just 2 cm below the junction of the right atrium and SVC.

Treatment / Management

Treatment of venous gas embolism is largely supportive. The first intervention should be discontinuing gasses, such as nitrous oxide, which may flow into the patient. One hundred percent O2 supplementation may correct hypoxia/hypoxemia and decrease the bubble's size due to a diffusion gradient allowing nitrogen to leave the gas embolus. Cardiac massage may be beneficial for severe venous gas embolism causing hemodynamic instability. Cardiac massage would move air out of the pulmonary outflow vasculature and into the smaller vessels, thus improving blood flow. If a catheter is already in place, such as a subclavian vein catheter, it is possible to advance the catheter into the heart and "suck out" the gas emboli. Positioning in the left lateral decubitus may be beneficial during this procedure to trap the emboli in the right heart for easier removal. However, no data supports the emergent placement of an intravenous catheter for venous gas embolism management if not already placed.[8][9][10] If the right heart function is compromised, inotropic agents such as dobutamine and ephedrine may be used. These agents increase preload to the left heart, improving cardiac output. 

While hyperbaric oxygen therapy is commonly used in arterial gas embolism, its use in venous gas embolism is not routine. Most patients with small venous gas embolisms have few if any, symptoms and do not require treatment. Generally, with smaller venous gas embolisms, the embolus eventually reaches the lungs, becomes trapped, and diminishes as the patient breathes. In cases of severe hemodynamic instability, hyperbaric oxygen therapy may be considered, but no data demonstrates benefit. If air embolism is suspected after chest trauma and the arrest does not respond to CPR, immediate thoracotomy and clamp of the hilum may need to be performed. However, this is a major undertaking with enormous morbidity and low survival rates. It should never be performed by a non-thoracic surgeon. 

Differential Diagnosis

The differential diagnosis for venous gas embolism includes the following:

• Heart failure
• Tension pneumothorax
• Septic shock
• Ischemic stroke

Prognosis

Most patients have no complications with a minute amount of air in the venous system. However, anytime air enters the CNS, the prognosis is grave. The patient's mental status, neurological deficits, and age are the 3 factors determining outcomes. There is always the potential for life-threatening complications with venous air embolism, especially if the air remains lodged into a vessel. Mortality rates of 30-80% have been reported following venous air embolism after chest trauma. Surgeons who perform procedures with the patient in the Fowler position or insufflate the body with carbon dioxide should remain extra vigilant as many cases of air embolism continue to be reported.