Air Embolism

Chapter 173 Air Embolism



Bonnie Wright, DVM, DACVA



KEY POINTS



• Air embolism occurs when a pocket of gas enters or is formed within the vascular compartment and subsequently forms an obstruction to blood flow.

• Intravenous catheter placement and use, laparoscopy, some surgeries, and hyperbaric therapies can all be associated with this complication.

• Prevention of air embolism is a priority because detection is difficult and tends to be delayed until after the embolism is dangerously large.

• Capnography and esophageal Doppler probes are the most useful tools for early detection of air embolism.

• Oxygen administration is recommended in patients with air embolism. Manual reduction involves aspirating the air from the embolus or reducing the size of air bubbles to allow perfusion around the bubbles.


INTRODUCTION


Because most veterinary patients do not scuba dive, air embolism is almost entirely an iatrogenic phenomenon in veterinary medicine. Because the simplest procedures, such as intravenous injection, have the potential to cause this calamity, it is important to consider the ramifications. The pathophysiology is determined by the size of bubbles and rate of intravenous gas entry.


Massive air embolism in the heart creates an absolute obstruction to blood flow; the compressible envelope of air contracts and expands with the working of the heart, and no blood gains entry to the air-filled chamber. Smaller air emboli wedge into vessels, creating focal areas of ischemia or leading to ventilation-perfusion mismatching if located in the lungs. With a continuous influx of air, small emboli coalesce into larger air pockets. Air emboli in the cerebral vasculature subject this vulnerable organ to hypoxemia, which, along with coronary artery emboli, marks the most severe consequence of small bubble gas embolization.


When an embolus is discrete enough to allow circulation to persist, gas is absorbed into the tissues, eventually reducing the volume of the embolism until it is completely dissolved or small enough to move to a more distal tissue bed. For this reason, the type of gas present in the bubble can have a tremendous impact on the amount of ischemia, as does the tissue bed in which the bubble becomes lodged. Administration of extremely insoluble gases (such as nitrous oxide) exacerbates gas emboli because the insoluble gas escapes from the blood and diffuses into the air pockets, causing expansion.1


Redundant blood flow salvages the lungs from significant damage from many small air emboli, and the lungs serve as the primary sponge for venous air emboli. A constant influx of air can overload this “filter” for emboli, allowing bubbles to emerge into the arterial system. In dogs, this occurs in 50% of animals when 0.35 ml/kg/min of air is infused.2 Furthermore, lodging of air emboli in the lungs is not necessarily benign and may cause focal injury, edema, and the subsequent release of vasoactive mediators. Eventually this can culminate in alveolar collapse, atelectasis, and impaired gas exchange.3



GAS EMBOLISM RESULTING FROM INTRAVENOUS ACCESS MISHAPS


In ordinary-sized patients, it is somewhat difficult to introduce enough air to create a clinically apparent embolism. Pigs have tolerated 2 ml/kg of air without irreversible hemodynamic collapse.1 However, pigs have a reduced ability to remove air during infusions when compared with dogs. Air delivery rate of only 0.1 ml/kg/min was associated with bubbles breaking through to the arterial system in pigs, whereas dogs tolerated up to 0.35 ml/kg/min.1,4 Extrapolating from the pig single-dose data, a 1-kg dog can probably tolerate up to approximately 2 ml of air as a single dose before cardiovascular collapse occurs.


The risk of air embolism is increased when venous access sites are located higher than heart level. This can occur in standing dogs and cats during jugular catheterization or puncture, or when ear catheters are used. Great care should be taken in placing jugular catheters in very small patients, in which a small amount of air could rapidly prove fatal.


In larger dogs and cats, embolization generally occurs when elevated catheters are left open to room air or become disconnected from a sealed system. Air moves into the relatively negative intravascular space, causing air entrainment with subsequent coalescence into a complete venous or cardiac obstruction. Because this usually occurs with patients in room air, the bulk of the embolus is composed of nitrogen gas. Nitrogen is relatively poorly soluble in tissues, so it takes several minutes for a nitrogen embolus to dissipate.5


Small air bubbles are often administered during intravenous injections and fluid therapy, but these are well tolerated in ordinary individuals. However, larger volumes of air may be mistakenly administered via intravenous tubing or extension sets that were not appropriately flushed, and in small patients this can be sufficient to cause irreversible damage.


Air emboli have also been known to form when intravenous fluid bags are placed under pressure. Most fluid bags contain a small amount of air that can be delivered when the entire contents of the bag are pressurized for rapid delivery to a patient. Increased caution is warranted in patients with a right-to-left cardiac shunt because the lungs may not filter out air bubbles; consequently these individuals may suffer from focal cerebral infarctions when even the smallest air bubbles are administered or allowed to form.

Related posts:

  1. Aspiration Pneumonitis and Pneumonia
  2. Myocarditis
  3. Left Ventricular Failure
  4. Shock Fluids and Fluid Challenge

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Air Embolism

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