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A 62-year-old male patient underwent pancreaticoduodenectomy with modified Child reconstruction for distal cholangiocarcinoma. After eight years, a contrast-enhanced computed tomography (CT) revealed a recurrent lesion at the biliojejunal anastomosis, and a biliary stent was placed for obstructive cholangitis in the right posterior segment of the liver. A right hepatectomy was planned for a local recurrent lesion;thus, percutaneous transhepatic portal embolization was performed on the portal vein's right branch to enlarge the left liver. However, he was referred to our department for endoscopic retrograde biliary drainage for the subsequent cholangitis and liver abscess appearance. A double-balloon enteroscope under CO 2 insufflation was used to reach the bile duct-jejunal anastomosis. After removing the bile duct stent with grasping forceps, his general condition suddenly deteriorated, causing cardiopulmonary arrest. He was diagnosed with air embolism based on the findings of air in the heart, aorta, and brain on CT after the return of spontaneous circulation. Treatment for the air embolism and subsequent complications continued in the intensive care unit, but he eventually died 114 days after the onset of the air embolism due to his deteriorating general condition. Pathological autopsy revealed cholangiocarcinoma that extends from the porta hepatis to the posterior segment. Additionally, the proximity between the bile duct and vein extended by the adenocarcinoma and the fibrous obstruction of the vein were revealed, indicating the possibility of a bile duct-vein shunt.

We designed this experiment to evaluate effects of intravenous bolus injection of air (0.5 ml.kg-1) on systemic blood pressure (SBP), central venous pressure (CVP), and renal nerve activity (RNA) in urethane-anesthetized rabbits. Animals were divided into the following three groups: animals with neuraxis intact (I group, N = 5), cervical vagotomized animals (V group, N = 5) and sinoaortic denervated animals (SAD group, N = 4). All animals were placed on the right-side down position to avoid effects of the posture throughout the experiments of air embolism. In the I group, air caused profound hypotension (from 95 +/- 10 to 54 +/- 15 mmHg) associated with a significant increase in CVP (from 2 +/- 2 to 7 +/- 3 mmHg) twenty seconds after the injection of air. In spite of the significant hypotension, RNA response did not show any increase for twenty seconds. This response was followed by an augmentation in RNA thirty seconds after air injection. In contrast, vagotomized animals exhibited a significant RNA increase (147 +/- 11% of the control) in response to a decrease in SBP (from 93 +/- 6 to 78 +/- 5 mmHg) and an increase in CVP ten seconds after the administration of air. In SAD group, a rapid and remarkable decline in SBP (from 85 +/- 13 to 47 +/- 12 mmHg) occurred ten seconds after the injection of air. Despite this hypotension, RNA decreased nearly to a noise level after administration of air.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of halothane, fentanyl and ketamine on the passage of air injected bolus across the pulmonary circulation was studied in dogs using transesophageal M-mode echocardiography. Dogs in Group 1 (N = 5) were anesthetized with halothane and then halothane with fentanyl. At least 3 weeks later the dogs were anesthetized with fentanyl and then fentanyl with halothane. The same procedure was utilized in group 2 (N = 4) using halothane and ketamine. The doses of halothane, fentanyl and ketamine were 1% inspired concentration, 100 micrograms.kg-1 followed by 1 microgram.kg-1.min-1 iv, and 10 mg.kg-1 followed by 0.1 mg.kg-1.min-1 iv, respectively. The threshold for bolus air detection during halothane, fentanyl and ketamine alone were 0.05, 0.5 and 0.2 ml.kg-1, respectively. The threshold during fentanyl administration, but not during ketamine administration, was significantly higher than that during halothane. The addition of halothane to fentanyl or ketamine lowered the threshold to the same level as with halothane alone, and the addition of either fentanyl or ketamine to halothane made no difference. Although there was no difference in baseline shunt fraction resistance index [PVRI/(Qs/Qt)] during administration of each anesthetic, every air injection decreased shunt fraction resistance index during halothane without fentanyl or during halothane with or without ketamine, and increased it during fentanyl administration.

Inducing pulmonary edema in rat, air bubbles the diameter of which was about 0.3 mm were continuously infused into the right atrium through a catheter at the rate of 2.8 ml/kg/hr during 0.5, 1 and 2 hours, under controlled ventilation (tidal volume of 9 ml/kg and respiratory rate of 80/min) with 1% halothane in room air. Saline or Dilazep hydrochloride solution was simultaneously infused into the right atrium via another catheter. Pulmonary edema was evaluated by the measurement of the ratio of extravascular water weight of lung (g) to blood-free dry lung weight (g) (EVWW) using the gravimetric method and with histologic studies using the rapid freezing method. In control rats, which were sacrificed immediately after induction of anesthesia, the EVWW was 3.114 +/- 0.121 g/g blood-free dry lung (mean +/- 1 S.D. n = 8). In baseline experiments (2 hours ventilation and saline infusion without air embolization), the EVWW was 3.291 +/- 0.081 (n = 4). In air embolization groups with 2 hours saline infusion, EVWW were 3.756 +/- 0.170 (n = 4), 3.722 +/- 0.170 (n = 4) and 3.731 +/- 0.245 (n = 5) in 0.5, 1 and 2 hours infusion groups, respectively. Regardless of emboli infusion time perivascular cuffs and peribronchial cuffs were revealed in the 2 hour saline infusion groups. In the experiment in which the animals were sacrificed immediately after one hour infusion of air bubbles, there was no evidence of pulmonary edema and the EVWW of 3.060 +/- 0.092 (n = 4) in this group control and baseline were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)