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CHAPTER 39: Pulmonary Embolic Disorders: Thrombus, Air, and Fat 333

points bear mention. It is clear that pharmacologic prophylaxis decreases TABLE 39-8 Etiology of Air Embolism
the risk of VTE in the ICU, 177,178 and thus most critically ill patients
should receive prophylactic heparin or LMWH. Mechanical prophylac- Surgery and Trauma Related Nonsurgical
tic strategies such as sequential compression devices are recommended if Upright neurosurgery Central line placement Cardiopulmonary
patients have a contraindication to prophylactic-dose anticoagulation. resuscitation
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Twice-daily unfractionated heparin was equally efficacious at reducing Liver transplantation Central line removal Gastrointestinal endoscopy
DVT compared to once-daily dalteparin, though the dalteparin group Total hip replacement Head/neck trauma
had significantly reduced rates of PE and of heparin—induced throm- Harrington rod insertion Dental implant surgery Barotrauma
bosis, leading some to advocate LMWH as the preferred prophylactic Spinal fusion Pacemaker insertion Positive-pressure ventilation
regimen. The use of IVC filters as a prophylactic strategy has not been Positive-pressure ventilation
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investigated, and most recommendations are to use only retrievable Pulsed saline irrigation Tenkhoff catheterization
filters for patients with known DVT who must interrupt anticoagulation, Tissue expander removal Intra-aortic balloon pump
and then to remove the filter once anticoagulation can be resumed. 179,181 Cesarean section Bone marrow harvest
Arthroscopy Epidural catheterization
AIR EMBOLISM
Open heart surgery Percutaneous lung biopsy
The syndrome of air (or gas) embolism results when air enters the vas- Hysterectomy Pulmonary contusion
culature, travels to the pulmonary circulation, and causes circulatory or
respiratory embarrassment. It is uncommonly recognized in critically ill Retrograde pyelography Laser bronchoscopy
patients, but is quite likely underdiagnosed. Hemodialysis Transurethral prostate resection
■ PATHOPHYSIOLOGY Percutaneous lithotripsy

The syndrome is triggered when a gas, usually air, enters a vessel, typi-
cally a vein. It travels with the venous return to the right heart and lungs,
where it may have circulatory or respiratory consequences. Occasionally, Respiratory Consequences: Air is carried into the pulmonary vasculature
air reaches the arterial circulation leading to systemic manifestations. where it embolizes in pulmonary arterioles and capillaries. The abnormal
Although air embolism is often abrupt and short-lived, intriguing cases of air-blood interface is thought to denature plasma proteins, creating amor-
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continuous streaming of bubbles in mechanically ventilated patients have phous proteinaceous and cellular debris at the surface of air bubbles.
been reported. At times, such embolism may persist over many days. This debris attracts and activates white blood cells, facilitating injury to
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the pulmonary capillaries. Endothelial injury increases capillary perme-
Entry of Air Into the Vasculature: Development of air embolism requires ability, which leads to alveolar flooding. The resulting noncardiogenic
an abnormal communication between air and the blood vessel. In pulmonary edema accounts for the majority of symptoms and signs due
addition, there must be a pressure gradient to favor entry of air into the to air embolism (see Chap. 52). In addition, air embolization leads to
vessel, rather than bleeding from the vessel. Trauma, surgical incisions, bronchoconstriction, a point which may be useful in diagnosis. 186
and intravascular catheters create the commonest sources of air entry. Although the dominant gas exchange abnormality is hypoxemia,
In addition, there are more subtle paths through which air can reach carbon dioxide elimination is impaired as well. As pulmonary vessels
the vasculature, such as in damaged, mechanically ventilated lungs of become occluded, alveoli subtended by them are ventilated, but unper-
patients with ARDS. The driving gradient for air entry may be provided fused. This increment in dead space may be signaled by a drop in ET ,
CO 2
by air under pressure, as during positive-pressure ventilation or high if this is being monitored. In the patient with fixed minute ventilation
pressure wound irrigation. Alternatively, the air may be at atmo- (eg, if the patient is muscle relaxed), P CO 2 will rise. Either of these may
spheric pressure, but the intravascular pressure is subatmospheric. For lead to suspicion of the diagnosis.
example, any vein which is above the heart by an amount exceeding the
right atrial pressure is likely to be at less than atmospheric pressure and Extrathoracic Manifestations: Air embolism is occasionally accompa-
therefore appears collapsed. For this reason, surgical sites above the nied by systemic findings. If air directly enters the pulmonary veins,
heart, particularly when the patient is in an upright or semirecumbent as may occur in patients being mechanically ventilated with acute
position, pose high-risk situations. Table 39-8 lists some of the causes lung injury, bubbles pass directly to the arterial circulation. However,
of the air embolism syndrome. since air typically enters a systemic vein, the arterial circulation is
protected from embolization by the filtering effect of the pulmonary
Circulatory Consequences: Massive air embolization can fill the right heart, circulation. Nevertheless, bubbles can pass to the left side of the heart
impede venous return, and thereby stop circulation. Thus, sudden death via the foramen ovale, which is probe patent in up to 30% of people.
is one of the possible outcomes. It is estimated that greater than 100 mL This type of foramen ovale does not ordinarily allow right-to-left
air must be acutely infused to arrest circulation. Most often, however, air shunting, due to the higher pressures in the left atrium. After signifi-
passes through the right heart into the lungs. There it raises Pa pressure, but cant embolization to the pulmonary circulation, however, right heart
has predominantly respiratory consequences. Since unilateral experimental pressures rise, reversing the inter-atrial gradient. This allows bubbles
air embolism causes pulmonary hemodynamic changes similar to bilat- to pass directly from the right to left atrium, then to the systemic
eral embolism, humoral or reflex vascular changes probably account for circulation. Even in the absence of a foramen ovale, air can reach the
some of the increase in pulmonary vascular resistance. In an experimental arterial circulation since the lungs do not fully filter air, especially
canine model of massive air embolism, systemic hypotension and pulmo- when a large amount is embolized. Air may pass through large extra-
nary hypertension were attenuated by pretreatment with an intravenous alveolar vessels or through the pulmonary capillaries themselves. In
endothelin-receptor antagonist. Such work suggests that the circulatory animal experiments, the threshold rate of venous air infusion which
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effects of air embolism may be due to cytokine release following release of overwhelms pulmonary filtering is 0.30 mL/kg per minute. For a
endothelin—a potent pulmonary vasoconstrictor—and that the activation 70-kg man, this value translates to only 21 mL/min.
of the cyclooxygenase pathway may contribute. One case study described Once air reaches the arterial circulation, peripheral embolization
a patient with suspected air embolism who developed the systemic inflam- leads to ischemic manifestations in the brain, heart, skin (livedo reticu-
188
matory response syndrome (SIRS), perhaps lending further credence to laris), and other organs. Some of the ischemic manifestations in the
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the idea that air in the circulation causes downstream humoral, not simply periphery are probably mediated by polymorphonuclear leukocytes
mechanical, consequences. and oxygen radicals, as is the injury in the lung. 189

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