Clinical Features of Venous Air Embolism
December 1, 2001
Clinical Features of Venous Air Embolism
The development of VAE related to CVC may be silent and of no clinical significance in the mildest form. Often, patients are described to have cough or deep breathing due to respiratory distress prior to development of VAE. A hissing sound of a large amount of air entry has been described in case reports. Numerous cases have been described where patients complain of dyspnea and an inability to catch their breath. With larger air emboli, hypoxia, cyanosis and tachycardia are noted. If the air embolism is massive, the patient may develop cardiorespiratory arrest. If circulation is somewhat maintained, sudden shock with signs of increased right-sided pressures in the form of elevated central venous pressures may develop. A "mill-wheel" murmur, due to churning of air inside the heart, has been described. Patients have been described who developed symptoms or signs of acute cardiac ischemia and infarction. Further systemic manifestations in the form of neurological changes are also known to develop. Depending on the circulatory involvement, any form of organ injury can be seen.
After acute onset, in mild cases, symptoms resolve quickly and this may be the only clue to the fact that the embolic manifestations were due to air. Rapid resolution of acute embolic events without therapy and without any evidence of thrombosis is often characteristic of air embolism. A large number of patients with moderate to massive air embolism develop pulmonary edema that typically resolves in 48 to 72 hours. Although the presentation of VAE can be dramatic and life threatening, rapid diagnosis and appropriate treatment often results in complete recovery. In most of the recently described cases as well as from personal observation, the diagnosis can be obtained by echocardiography. This is true especially in the operating room. Demonstration of air bubbles in central veins or major arteries or in the cardiac chambers is diagnostic. A rapid drop in end-tidal CO2 is another sign of this embolic phenomenon, and in appropriate settings it can be diagnostic.
Treatment
Acute Massive VAE. When VAE is suspected as the cause of cardiac arrest or acute cardio-respiratory compromise, the patient should be immediately placed in the left lateral decubitus and Trendelenburg positions. This patient position makes the right ventricle the highest cardiac structure. Air, being lighter than blood, moves to the top of the right ventricle and is described to relieve the right ventricular outflow tract and may result in re-establishment of circulation. Further, if the diagnosis is made with echocardiogram immediately or is strongly suspected, air can be aspirated through the distal port of the CVC as well. Also, if an obvious source of air entry is found, appropriate measures should be taken to prevent further air entry into the circulation. Once the circulation is established general treatment strategies are used. In patients with cardiorespiratory arrest, appropriate advanced cardiac life support measures have to be taken.
General Measures
Oxygen. Even if patients are not hypoxemic, 100% oxygen therapy is recommended in patients with VAE. Dissolved oxygen can perhaps result in oxygenation of areas where blood flow is diminished due to obstruction by an air bubble. Also, oxygen can directly be exchanged for small amounts of nitrogen resulting in decrease in size and increase in surface tension on the air bubble that may result in faster resolution of air embolism.
Circulatory Support. If the patient remains hypotensive, infusion of saline should be considered. It is postulated that a drop in hematocrit due to fluids would be associated with decrease in viscosity of blood and that decreased viscosity may be favorable when there is micro-circulatory obstruction.
Hyperbaric Oxygen Therapy. In severely hypoxic patients or in patients with severe clinical manifestations, hyperbaric oxygen therapy can be considered once stable hemodynamics are achieved. Increasing atmospheric pressure directly reduces the size of the air bubble and results in break down of larger bubbles that obstruct vasculature. Also, significantly larger amounts of dissolved oxygen become available both for exchange with the air bubbles and also for oxygen delivery to areas where hemoglobin inside the red blood cell can not reach but plasma can diffuse. An arterial PO2 of > 1000 mm Hg can be achieved under hyperbaric conditions, making the dissolved oxygen a significant contributor to overall oxygen transport.
Controversial Therapies. Heparin, lidocaine and high-dose corticosteroids have been used in the past to treat VAE, especially if there are CNS manifestations. However, their role remains unproven and controversial at best.
Prevention of VAE Related to CVC
The use of the Trendelenburg position is strongly recommended both during insertion and removal of CVCs from either jugular or subclavian locations. When a large bore catheter is exchanged with small-bore catheter, care should be taken to occlude the orifice at skin level as best as possible. When a CVC is removed, an occlusive dressing should be applied at the site of the catheter. If patients are discharged with CVC, due care should be explained especially highlighting the need to keep the catheter capped at all times. Although these preventive measures seem obvious, a recent nursing survey found that a large number of CVCs were removed when patients were not in Trendelenburg position, and sometimes when patients were in sitting position.
Summary
In summary, VAE related to CVC is largely a preventable complication that can present with varied clinical manifestations. Prompt recognition and appropriate treatment including oxygen therapy and hyperbaric oxygen therapy may result in complete recovery.
References
1. Dumont CP. Procedures nurses use to remove central venous catheters and complications they observe: A pilot study. Am J Crit Care. 2001;10(3):151-155.
2. Kashuk JL, Penn I. Air embolism after central venous catheterization. Surg Gynecol Obstet. 1984;159(3): 249-252.
3. Muth CM, Shank ES. Gas embolism. N Engl J Med. 2000;342(7):476-482.
4. Orebaugh SL. Venous air embolism: Clinical and experimental considerations. Crit Care Med. 1992;20(8):1169-1177.
You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content