1Department of Anesthesiology and 2Department of Cardiology, Ajou University, School of Medicine, 5 Wonchon-Dong, Paldal-Gu, Suwon 441-749, Korea* Corresponding author
Accepted for publication: September 5, 2001
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Abstract |
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Br J Anaesth 2002; 88: 1368
Keywords: liver, resection; embolism, air
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Introduction |
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Case report |
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Hepatic resection using electrocautery and ultrasonic dissector was started after clamping the branches of the portal vein and the right hepatic artery supplying the right lobe of the liver.
Two hours and 20 min after the start of operation, an abrupt decrease in FE'CO2 (from 32 to 15 mm Hg) and SpO2 (from 100% to below 60%) were noted. The administration of N2O was immediately discontinued and the patients lungs were hyperventilated with 100% oxygen. After a few seconds, systolic arterial pressure decreased from 120 mm Hg to under 20 mm Hg and heart rate fell from 65 beats min1 to less than 20 beats min1 with severe ST depression on ECG monitoring. Embolism was suspected. The infusion tubing was checked, and was found to be satisfasctory. The surgeons acknowledged that a large number of small hepatic veins were cut and open to the atmosphere. The patients position was changed from supine to left lateral decubitus, and ephedrine 12 mg, atropine 0.4 mg and epinephrine 100 µg given through the central venous catheter. When cardiovascular measurements improved, arterial blood gas analysis showed PaO2 161 mm Hg and PaCO2 34 mm Hg with FIO2 of 1.0. About 510 min after the onset of clinical signs,a TOE probe was placed. Air bubbles were seen coming from the right pulmonary vein into the left atrium (Fig. 021F1). No right-to-left intracardiac shunt was found by colour flow echocardiography. Although the number of air bubbles decreased progressively, they continued to appear in the left heart from the right pulmonary vein for 20 min. During this time no air bubbles were seen in the right heart (Fig. 021F2). These findings suggest that embolism had occurred from cut small hepatic veins being exposed to the air, and passed through dilated pulmonary vessels and appeared in the left heart.
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Hyperventilation was continued with 100% oxygen. An infusion of low dose dobutamine was given until the air bubbles had disappeared. At the end of surgery (1 h after the reduction of FE'CO2), PaO2 was 395 mm Hg and PaCO2 was 43 mm Hg with FIO2 of 1.0. The patient was extubated 3 h later in the intensive care unit, and the early postoperative course in intensive care unit was satisfactory. There was no clinical evidence of pulmonary oedema or neurological sequelae.
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Discussion |
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VAE is unlikely to occur in patients undergoing abdominal procedures while in the supine position, unless the inferior vena cava or pelvic veins are exposed to the air.9 10 However, during hepatic resection, vena cava manipulation or compression may narrow its diameter at the junction with the hepatic veins. In such a situation, the venous distending pressure of the constricted portion of the inferior vena cava may be less than in the nonconstricted part, and becomes even subatmospheric when blood passes through the narrowed portion with a high flow rate. Air could be sucked into the inferior vena cava via the large number of small hepatic veins exposed to the atmosphere.1 In our case, the inferior vena cava was being compressed while a large number of small hepatic veins were open to the air.
The effects of air embolism depend on the volume as well as the rate of air entry. Adornato et al.11 reported that slow infusion of air (0.01 to 2.00 ml kg1 min1) passes through the right side of the heart, occludes the pulmonary circulation and causes a progressive increase in CVP, an abrupt increase in pulmonary arterial pressure (PAP) to a plateau and a progressive decrease in peripheral resistance. The reduced resistance may be compensated for by an increase in cardiac output but hypotension can follow when compensation fails. In contrast, injection of a bolus air (25200 ml; 113 ml kg1) occludes the right side of the heart, increases CVP, decreases PAP, and causes hypotension. Many clinical episodes of VAE result from combinations of slow infusion and also introduction of larger amounts. In our case, CVP and PAP were not measured during resuscitation but we noted ST depression, shock and brodycardia. This suggests that a large volume was introduced.
Various methods can be used to prevent embolism. An increase in venous pressure by using PEEP might reduce entrainment of air into the circulation or stop air entrainment after air embolism has been detected.12 This is controversial because an increase in venous pressure might cause paradoxical embolism if the patient had a right-to-left shunt.13 We used 3 cm H2O of PEEP and, this was reduced during resuscitation. Another method to prevent VAE is changing position during operation. During the parenchymal phase of the operation, some suggest that the patients should be in a Trendelenburg position of about 15°.14 In our case, the patient was supine, since we have done about 200 cases of major hepatic resection with this position without previous incident.
When VAE has developed, a position of head-down and left lateral decubitus can protect from embolism effects.11 In our case, after the reduction of FE'CO2, the lateral decubitus position was used because we suspected slow entry of the air.
PAE occurs when the air in the venous system or in the right heart passes through an intracardiac channel and reaches the systemic circulation. A persistent patent foramen ovale exists in 1035% of the population and is the most common route for PAE.15 However, air may also reach the systemic circulation through pathological dilatation of intrapulmonary vessels normally present in some people (but more frequent in end-stage liver disease).16 In the normal individual, pulmonary parenchymal precapillary and capillary blood vessels have a diameter of 815 µm.17 However, in patients with chronic liver diseases, intrapulmonary shunting can occur by intrapulmonary vascular dilatation (up to 160 µm) at the precapillary level, or by direct arteriovenous communications.17 18 Hopkins et al.3 reported that 47% of cirrhotic patients had right-to-left intrapulmonary shunting, shown by contrast echocardiography. In this case, TOE demonstrated air bubbles passing from the right pulmonary vein into the left atrium. No right-to-left intracardiac shunt could be detected by colour flow echocardiography. These findings suggest that the source of PAE was from dilated pulmonary vasculature and not from an undignosed intracardiac shunt.
TOE and precordial Doppler ultrasound are the most sensitive modality in detecting VAE5 and can discriminate intracardiac from transpulmonary passage.68 In patients with intracardiac communications, immediate opacification of the left heart chambers occurs after arrival of air into the right heart chambers. However, in patients with transpulmonary passage, air passes into the pulmonary circulation where it is trapped in capillaries with diameter of 815 µm. It is either absorbed into alveolar space or dissolved during pulmonary transit, if the size of bubbles are less than 8 µm in diameter.19 When pulmonary vessels are dilated at the pre-capillary level (>15 µm), delayed opacification in the left atrium occurs approximately three to six ventricular contractions after leaving the right ventricle.6 In this case, we placed a transoesophageal probe about 510 min after the onset of signs and air bubbles were still seen arriving in the left atrium via the right pulmonary vein. An intracardiac shunt was not seen. These findings suggest pulmonary vasodilatation.
Intrapulmonary shunting is implicated in the pathophysiology of the hypoxaemia observed in patients with chronic liver disorders.20 However, three out of five patients with vascular dilatation had PaO2 values of 82 mm Hg or more while breathing room air.4 In our case, the patient was not hypoxic before the operation.
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References |
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